Biomedical subjects

M G Grace

Publications and source records attributed to M G Grace.

At least 37 records · Page 2Linked to original sources

PubMed1992

Effect of intrathecal superoxide dismutase and catalase on oxyhemoglobin-induced vasospasm in monkeys.

A gel consisting of agarose and oxyhemoglobin (OxyHb) was developed so that, when placed in the subarachnoid space, OxyHb would be slowly released, simulating lysis of erythocytes after subarachnoid hemorrhage. The system was used to investigate the importance of reactions mediated by free radicals in the genesis of OxyHb-induced vasospasm in monkeys. Seventeen monkeys were randomly assigned to have subarachnoid placement, on Day 0, of one of the following: 1) agarose gel alone (n = 2); 2) agarose plus OxyHb (n = 3); 3) agarose plus OxyHb plus intrathecal administration of superoxide dismutase and catalase (n = 6); and 4) agarose plus OxyHb plus intrathecal administration of placebo (n = 6). Vasospasm was assessed by comparison of angiograms performed on Day 0 and 7 days after subarachnoid placement of compounds, and by electron microscopy. OxyHb alone caused significant reduction in the diameter of the middle cerebral artery (40 +/- 8%, P less than 0.005, paired t test), which was associated with ultrastructural damage to smooth muscle. Treatment with superoxide dismutase plus catalase or with placebo attenuated vasospasm of the middle cerebral artery, although significant narrowing persisted in both groups (27 +/- 12% and 26 +/- 13%, respectively, P less than 0.05, paired t test). Analysis of variance showed no difference in the degree of vasospasm between groups exposed to subarachnoid placement of OxyHb. Cerebrospinal fluid aspirated from the cisterna magna on Day 7 contained elevated activity of superoxide dismutase in animals that received treatment. Malondialdehyde was undetectable in cerebrospinal fluid after subarachnoid placement of agarose alone, although it was present in similar amounts in all groups that received subarachnoid placement of OxyHb. Since intrathecal superoxide dismutase and catalase failed to protect against OxyHb-induced vasospasm, mechanisms mediated by free radicals may not be important in its genesis. As only one combination of doses of superoxide dismutase and catalase was administered, however, it may be that other dosage schedules might be efficacious.

Animals↗

PubMed1992

Cytoskeletal and extracellular matrix proteins in cerebral arteries following subarachnoid hemorrhage in monkeys.

It is unclear if vasospasm after subarachnoid hemorrhage (SAH) is predominantly due to smooth-muscle contraction, proliferative vasculopathy, or other changes within the arterial wall such as fibrosis or change in smooth-muscle phenotype. In this study, immunohistochemistry was used to examine changes in extracellular and cytoskeletal proteins in cerebral arteries after SAH that might support one of these mechanisms. Following baseline cerebral angiography, bilateral SAH was created in nine monkeys. Three animals each were killed 7, 14, or 28 days after SAH. Cerebral angiography was repeated on Day 7 in all animals and immediately prior to sacrifice in animals killed on Days 14 and 28. Both middle cerebral arteries and four control basilar arteries were examined using fluorescent antibody techniques with antisera to alpha-actin, myosin, fibronectin, fibrinogen, vimentin, desmin, laminin, and collagens (types I, III, IV, and V). Angiography showed that vasospasm was most severe on Day 7, present but resolving on Day 14, and completely resolved by Day 28. Microscopic study of arterial sections and blinded review of microphotographs of arterial sections by five independent observers did not reveal changes in intensity of density of staining for collagens, desmin, myosin, laminin, or alpha-actin in the tunica media of tunica adventitia. Fibronectin immunoreactivity increased 14 days after SAH. Seven days after SAH, occasional areas of tunica media showed immunoreactivity to fibrinogen. On Day 28, intimal thickening was observed in four of six middle cerebral arteries and this tissue demonstrated immunoreactivity to alpha-actin, myosin, vimentin, desmin, fibronectin, laminin, and each type of collagen. No significant increases in the number of intimal cells showing immunoreactivity to alpha-actin were seen and no significant changes in the hydroxyproline content of cerebral arteries developed at any time after SAH. These results suggest that rigidity and lumen narrowing of vasospasm are not due to increased arterial collagen, although other proteins in the arterial wall or an alteration in cross-linking of existing proteins could produce these changes. There is no indication that smooth-muscle contractile proteins change during vasospasm or that increases in the number of alpha-actin-containing myointimal cells contribute to vasospasm. The occurrence of intimal thickening and increased tunica media fibronectin after vasospasm suggests that vasospasm damages smooth muscle, possibly as a result of intense prolonged smooth-muscle contraction.

Animals↗

PubMed1992

Malondialdehyde, glutathione peroxidase, and superoxide dismutase in cerebrospinal fluid during cerebral vasospasm in monkeys.

Cerebral vasospasm may result from lipid peroxidation induced by oxyhemoglobin in the subarachnoid space after subarachnoid hemorrhage. To test this theory, vasospasm was induced in monkeys by intrathecal injections of oxyhemoglobin or supernatant fluid from autologous blood incubated in vitro. Concentration of malondialdehyde (MDA), a product of lipid peroxidation, was elevated in cerebrospinal fluid (CSF) in association with vasospasm caused by oxyhemoglobin and supernatant fluid. Intrathecal injections of methemoglobin or bilirubin did not cause vasospasm or increased CSF MDA. Activity of glutathione peroxidase in CSF increased significantly after injection of oxyhemoglobin and methemoglobin. There were no significant changes in CSF superoxide dismutase activity although there was a trend towards higher activities in animals treated with oxyhemoglobin, methemoglobin, bilirubin, and supernatant fluid. These results show oxyhemoglobin-induced vasospasm is associated with MDA and lipid peroxidation in the subarachnoid space. Furthermore, detection of peroxidation products after injection of oxyhemoglobin in the absence of erythrocyte membranes indicates that oxyhemoglobin may directly damage cerebral arteries and brain by inducing lipid peroxidation in these structures. Depletion of free-radical scavenging enzymes in CSF did not seem necessary for development of vasospasm. In fact, there was a tendency for vasospasm to elevate enzyme activities, as if production of scavengers was induced by excess free radicals in the subarachnoid space.

Animals↗

PubMed1992

Mechanism of cerebral vasospasm following subarachnoid hemorrhage in monkeys.

This paper reviews our recent studies on the mechanism of cerebral vasospasm following subarachnoid hemorrhage (SAH) in monkeys. Middle cerebral artery (MCA) vasospasm was maximal at 7 days, resolving by 14 days, and absent at 28 days after SAH. Arterial fibrosis was not detected during vasospasm, although there was intimal hyperplasia with fibrosis 28 days after SAH. On scanning electron microscopy, smooth muscle cells from vasospastic arteries had corrugated cell membranes and appeared similar to cells contracted pharmacologically, suggesting that vasospastic smooth muscle is contracted. Morphometric analysis of arteries obtained 7 days after SAH showed no significant increases in arterial wall area of vasospastic arteries compared with normal MCAs. The results suggest vasospasm in monkeys is not due to hypertrophy, hyperplasia, or fibrosis in the arterial wall. Vasospasm may be mainly vascular smooth muscle contraction, which damages the arterial wall, leading to secondary structural changes in the arterial wall which occur after angiographic vasospasm.

Animals↗

PubMed1992

A survey of vertebral burst-fracture management in Canada.

In the management of burst fractures, the role of direct surgical removal of retropulsed bony fragments encroaching upon the spinal canal (direct decompression) is controversial. A questionnaire was mailed to 65 neurosurgeons and 36 orthopedic surgeons across Canada to determine the current management of vertebral burst fractures and the willingness of these surgeons to participate in a longitudinal study of the effects of direct surgical decompression in the management of burst fractures. Sixty-nine (44 neurologic and 25 orthopedic) surgeons responded to the questionnaire. Of those who responded, 97% of the neurologic surgeons and 95% of the orthopedic surgeons stated that they used plain radiography and computed tomography in their pretreatment investigations, and at least 50% in each specialty repeated these investigations at follow-up examinations. Standard tomography, magnetic resonance imaging and myelography were used less frequently both before and after surgery. There were no significant differences between specialties in the use of tests. Neurologic status and the treating surgeon's specialty were found to significantly influence management of burst fractures. According to 56% of neurologic surgeons and 81% of orthopedic surgeons, neurologically intact patients were usually treated with stabilization only (p less than 0.05). The greater number of neurosurgeons who used direct decompression was balanced by the number of orthopedic surgeons who used indirect decompression. Patients with partial, stable neurologic injuries were usually managed by direct decompression and stabilization according to 84% of the responding neurologic surgeons and 77% of the responding orthopedic surgeons.(ABSTRACT TRUNCATED AT 250 WORDS)

Canada↗

PubMed1991

Spine trauma and associated injuries.

A longitudinal, prospectively gathered data base of spine trauma has been developed. A review of 508 consecutive hospital admissions identified the presence of associated injuries in 240 (47%) individuals, most frequently involving head (26%), chest (24%), or long bones (23%). Twenty-two per cent had one associated injury, 15% had two, and 10% had three or more. Most spine fractures involved the lower cervical (29%) or thoracolumbar junction (21%). Comparisons of presence or absence of associated injuries and spine fracture level showed significant differences (p less than 0.001). Eighty-two per cent of thoracic fractures and 72% of lumbar fractures had associated injuries compared to 28% of lower cervical spine fractures. While there was no significant relationship between type of associated injury and spine fracture level, those with associated injuries were less likely to have a neural deficit (p less than 0.05). After hospital admission, there were seven deaths. Early assessment and transport of spine trauma victims must be carried out with appropriate management of associated injuries. Conversely, multiple trauma victims must be handled with due regard for a possible spine fracture. The value of spinal units with specially trained personnel is emphasized.

Adult↗

PubMed1991

Scanning electron microscopy of normal and vasospastic monkey cerebrovascular smooth muscle cells.

Normal cytoarchitecture of smooth muscle cells of monkey cerebral arteries was studied using scanning electron microscopy after removal of adventitial connective tissue by hydrolysis with HCl. Cerebral arteries were also examined after contraction in vitro with prostaglandin F2 alpha (PGF2 alpha). Anterior cerebral arteries were studied after exposure for 6 days in vivo to whole blood, oxyhemoglobin, methemoglobin, bilirubin, mock cerebrospinal fluid, or supernatant fluid from an incubated mixture of autologous blood and mock cerebrospinal fluid. Normal smooth muscle cells were spindle-shaped and oriented circumferentially around the vessel. They were often grouped into bundles of 5 to 10 cells; bundles were recognizable because cells within them were joined by multiple intercellular contacts. Groups of smooth muscle cells oriented longitudinally were present outside the circular layers of cells. The adventitial surface of muscle cells was smooth apart from fine longitudinal striations in some areas. Arteries contracted with PGF2 alpha had markedly convoluted and folded cell membranes. Muscle cells of vasospastic arteries and of arteries exposed to oxyhemoglobin and supernatant fluid appeared identical to cells contracted with PGF2 alpha. The outer surface of cells of arteries exposed to bilirubin, methemoglobin, and mock cerebrospinal fluid were normal. Marked similarity between vasospastic smooth muscle cells and smooth muscle cells from arteries contracted with PGF2 alpha suggest that smooth muscle contraction occurs during "vasospasm" due to whole blood and to intrathecal injection of oxyhemoglobin.

Animals↗

PubMed1991

Morphometric analysis of monkey cerebral arteries exposed in vivo to whole blood, oxyhemoglobin, methemoglobin, and bilirubin.

Whether vasospasm results from smooth muscle contraction or from arterial wall infiltration by cells and other material is subject to debate. Computer-assisted image analysis was used to measure lumen area, total wall area, and area of tunica media plus tunica intima of cross-sections of monkey right middle cerebral arteries (MCAs), exposed in vivo for 6 days to whole blood (n = 4), oxyhemoglobin (OxyHb, n = 5), methemoglobin (MetHb, n = 5), bilirubin (n = 5), mock cerebrospinal fluid (CSF, n = 6), and supernatant fluid from an incubated mixture of autologous blood and mock CSF (n = 5). Five control (left) MCAs from each group and 4 MCAs contracted in vitro with potassium chloride were measured. Significant angiographic vasospasm occurred in groups receiving whole blood, supernatant fluid, and OxyHb (p less than 0.05). There was significant correlation (r = 0.58, p less than 0.05) between right MCA diameter on angiography and diameter calculated from lumen area. When compared to effects of mock CSF, OxyHb significantly increased total wall area. When right and left MCAs were compared within groups, total wall area increased in every group with significant increases in groups exposed to mock CSF, OxyHb, and bilirubin (p less than 0.05). No changes developed in area of tunica media plus tunica intima, whether comparing right versus left MCAs within groups or right MCAs between groups. Contraction in vitro did not significantly increase total wall area or area of tunica media plus tunica intima. Light microscopy demonstrated inflammatory debris in the tunica adventitia of arteries from every group. This study shows that whole blood, OxyHb, and supernatant fluid, which contains OxyHb, cause vasospasm. Increases in total wall area are not sufficient to account for luminal narrowing, and therefore, changes such as cell proliferation and arterial wall fibrosis in the intima or media apparently do not contribute primarily to arterial narrowing of vasospasm but could be related to persistence of narrowing. Vessel wall thickening, which does occur, is caused by increased tunica adventitia area only and is nonspecific in that it develops after injection of substances not associated with vasospasm. The data are consistent with the hypothesis that oxyHb causes vasospasm (both angiographic and morphologic) by inducing muscle contraction in the media.

Animals↗

PubMed1991

Intracisternal recombinant tissue plasminogen activator after aneurysmal subarachnoid hemorrhage.

Fifteen patients undergoing surgery within 48 hours of aneurysm rupture were administered recombinant tissue plasminogen activator (rt-PA) directly into the basal subarachnoid cisterns after minimal surgical clot removal and aneurysm clipping. Preoperatively, 13 patients had diffuse or localized thick subarachnoid blood clots on computerized tomography (CT), and two had diffuse thin clots. The rt-PA was given as a single intraoperative injection of 7.5 mg (one patient), 10 mg (nine patients), or 15 mg (five patients). Postoperative cisternal drainage was employed in three patients. All patients except one demonstrated partial to complete cisternal clot clearance on CT scans within 24 hours after surgery. The patient who showed no clot reduction was the only patient in this series to develop symptomatic vasospasm and was the only fatality, dying 8 days after rupture. No vasospasm was seen on follow-up cerebral angiography in six of the 14 responding patients, and mild-to-moderate arterial narrowing was seen in at least one major cerebral artery in the remaining eight patients. Severe angiographic vasospasm was not seen, although the patient who died did not undergo repeat angiography. There was one major complication early in the series which seemed clearly related to treatment, and that was a large extradural hematoma occurring within several hours of craniotomy. Intrathecal fibrinolytic treatment appears effective in clearing subarachnoid clot and reducing vasospasm, and may be associated with acceptable risks if given to patients with large-volume subarachnoid hemorrhages at high risk for severe vasospasm.

Adult↗

PubMed1991

Etiology of cerebral vasospasm in primates.

A primate model was used to determine whether oxyhemoglobin (OxyHb), methemoglobin (MetHb), or bilirubin is likely to be responsible for cerebral vasospasm following subarachnoid hemorrhage (SAH). Forty cynomolgus monkeys were randomly assigned to one of five groups. On Day 0, each animal underwent angiography followed by right craniectomy and placement of an Ommaya reservoir with its catheter adjacent to the right middle cerebral artery (MCA). The animals received intrathecal injections twice a day for 6 days of one of the following solutions: mock cerebrospinal fluid (CSF); OxyHb; MetHb; bilirubin; or supernatant fluid from an incubated mixture of autologous blood and mock CSF. On Day 7, angiography was repeated and the animals were killed. Comparison of angiograms obtained on Day 0 and Day 7 of the experiment showed significant vasospasm of the right MCA and the right anterior cerebral and internal carotid arteries in the animal groups that had received OxyHb or supernatant fluid. There was a smaller reduction in diameter of the same vessels in the bilirubin group (not statistically significant), while no effects were observed in the groups receiving MetHb or mock CSF. Electron microscopy of the right MCA's gave results consistent with the angiographic findings. One monkey in the OxyHb group developed a delayed-onset right MCA infarction. These data suggest that OxyHb is the cause of cerebral vasospasm following SAH.

Animals↗

PubMed1991

Surgical manipulation of primate cerebral arteries in established vasospasm.

It is generally believed that surgery in the face of angiographic vasospasm is dangerous due to an increased incidence of postoperative cerebral ischemia. One theory is that arterial narrowing is exacerbated by surgical manipulation of vasospastic vessels during aneurysm dissection and clipping. This theory was tested in a primate model of cerebral vasospasm and the results reported. Six monkeys underwent baseline cerebral angiography, followed by induction of subarachnoid hemorrhage (SAH) on both sides of the circle of Willis. An equal amount of fresh autologous blood clot was placed around each internal carotid, anterior cerebral, and middle cerebral artery. Six days later, angiography was repeated and the right craniectomy was reopened for clot evacuation and surgical manipulation of the right cerebral arteries, including placement of a temporary aneurysm clip on the right middle cerebral artery. The left cerebral arteries were not exposed or manipulated, and served as controls. Twenty-four hours later angiography was repeated, then the animals were killed. Equal and significant vasospasm (greater than 40% reduction in vessel caliber compared to baseline, p less than 0.05) was seen in the middle cerebral arteries on both sides of the circle of Willis in all animals 6 and 7 days after SAH. There was no significant change in the severity of vasospasm on Day 7 compared with Day 6 in the right cerebral arteries. Increased risk of postoperative cerebral ischemia for surgery in the peak vasospasm period may be due to mechanisms other than increased arterial narrowing precipitated by surgical manipulation.

Animals↗

PubMed1990

Predictive equation for assessing energy expenditure in mechanically ventilated critically ill patients.

Traditional formulas, such as the Harris and Benedict equation (HBE), do not accurately predict energy expenditure (EE) in mechanically ventilated, critically ill patients (MVCIP). The purpose of this study was to develop a predictive EE equation to assess EE requirements in MVCIP. A portable metabolic cart was used to measure indirectly EE in 112 MVCIP. Patients were studied at rest and for 30 min on the first or second day of ICU admission. No nutrition was received during the study period. Variables investigated were: age, BSA, Acute Physiology and Chronic Health Evaluation (APACHE II) score, sepsis score, Injury Severity Score (ISS), respiratory rate (f), tidal volume (VT), minute ventilation, mean arterial pressure, heart rate, body temperature (Temp), and outcome. Patient age, APACHE II score, sepsis score, ISS, and BSA were 50 +/- 20 yr, 16 +/- 7, 11 +/- 6, 32 +/- 14, and 1.80 +/- 0.27 m2, respectively. Correlation and multiple regression analyses were used with EE as the dependent variable. A predictive equation (EE [kcal/day] = 945 BSA -6.4 age + 108 Temp + 24.2 f + 817 VT -4349) was determined from variables that contributed greater than 3% to the variance of EE: BSA (52%), age (10%), f (5%), VT (5%), and Temp (3%). The HBE underestimated measured EE by 34 +/- 19% and in 79 patients deviated greater than 15%. Using the new equation, only 15 patients' EE deviated greater than 15% from measured EE. The new predictive EE equation can accurately assess EE in MVCIP.

Adult↗

PubMed1990

Tisseel, a two component fibrin tissue sealant system: report of a trial involving anticoagulated dental patients.

There have been attempts since the early years of this century to produce a biocompatible, biodegradable tissue glue to aid in hemostasis and lessen the need for conventional sutures. In the early 1970s, Matras et al developed a glue to anastomose the severed ends of peripheral nerves, and which was the precursor of the product tested in this trial. Since that time, the product has gained wide acceptance in Europe, with applications in microvascular anastomosis, hemostasis of soft tissue defects, bone sealing and dural sealing.

Anticoagulants↗

PubMed1989

Burn injuries in native Canadians: a 10-year experience.

Between 1977 and 1986, 1598 patients were admitted to the Firefighters' Burn Unit of the University of Alberta Hospital in Edmonton, Alberta. One hundred and twenty-five (7.8 per cent) of these patients were Treaty Indians or Metis compared to 4.2 per cent of the general population in the same given area. The data show native people suffered larger total body surface area (TBSA) burns, were hospitalized on average 16.9 days longer and required 0.7 more operations than their non-native counterparts. Natives are also three times more likely to remain within the health care system as inpatients for rehabilitation after acute burn management has been completed. Mortality rates as a result of these burns were similar for natives (4.8 per cent) and non-natives (4.3 per cent). This review indicates that the native population is at higher risk of suffering burn injury even after adjusting for certain demographic variables, consequently impacting the utilization of the health care system.

Adolescent↗

PubMed1989

School performance of survivors of neonatal encephalopathy associated with birth asphyxia at term.

School performance testing was completed at 8 years of age on 145 children who had had neonatal encephalopathy associated with birth asphyxia as term infants and on a comparison peer group of 155 children. The prospectively identified clinical categories of encephalopathy for the neonates were 56 mild (hyperalertness, hyperexcitability), 84 moderate (lethargy, hypotonia, suppressed primitive reflexes), and 5 severe (stupor, flaccidity, absent primitive reflexes). The mortality rate to 8 years of age was 13%. The incidence of impairment, which included cerebral palsy, blindness, cognitive delay, convulsive disorder, and severe hearing loss, was 16% among those assessed at 8 years (75% of survivors). Intellectual, visual-motor integration, and receptive vocabulary scores, as well as reading, spelling, and arithmetic grade levels for those with moderate or severe encephalopathy, were significantly below (p less than 0.01) those in the mild encephalopathy or peer comparison groups. Predictors of reading performance for the study group included category of encephalopathy, birth weight for gestational age, native language, and mother's educational level (multiple R = 0.58). Nonimpaired survivors of moderate encephalopathy were more likely to be more than one grade level delayed than were children from the peer group (reading 35% vs 15%, spelling 18% vs 8%, arithmetic 20% vs 12%, p less than 0.01). Thus children who had moderate and severe neonatal encephalopathy are at risk for physical and mental impairment and reduced school performance. Children with mild encephalopathy had school performance scores similar to those of their peers.

Asphyxia Neonatorum↗

PubMed1989

Early prognosis for ambulation of neonatal intensive care survivors with cerebral palsy.

The ambulatory status of 74 neonatal intensive care unit survivors with cerebral palsy, excluding those with central nervous system malformations and syndromes, was assessed at eight years of age. Detailed examinations were completed at two and eight years of age; of the 47 who were sitting by two years, 46 became ambulatory, and a total of 47 of the 74 children became ambulatory. The clinical type of cerebral palsy at two years of age related significantly to eight-year ambulation. However, between two and eight years the diagnosis was changed for 18 children. At two years of age the tonic labyrinthine, asymmetrical and symmetrical tonic neck and Moro reflexes related significantly to ambulation; in five of 27 children not walking, these reflexes were absent by two years of age. Foot placement and/or parachute reactions at two years were found in more than one-third of children not walking. Multivariate analysis determined that age at sitting explained 91 per cent of the variance in ambulation. No other variables, combined with sitting, increased this prediction.

Ataxia↗

PubMed1988

Intrathecal nimodipine therapy in a primate model of chronic cerebral vasospasm.

The safety, prevention, and treatment of chronic vasospasm by repeated administration of intrathecally applied nimodipine was evaluated in a primate model of chronic cerebral vasospasm. Twenty-four female cynomolgous monkeys were randomized into three groups of 8: sham, clot, and clot + intrathecal nimodipine. All animals underwent a subarachnoid hemorrhage (SAH) induction operative procedure after base line angiography. Nimodipine was administered postoperatively by subcutaneous injection of 1 ml/0.2 mg tid for 6 days through an Ommaya reservoir with the catheter placed in the subarachnoid basal cisterns. Angiography was performed on Day 7 post-SAH induction. Intrathecally applied nimodipine was not effective in the prevention of angiographic vasospasm. It also did not seem to decrease the degree of pathological change when compared to controls. One animal in the nimodipine group died 2 hours after an intrathecal injection secondary to a respiratory arrest. Transient sedation and hypoventilation were common. No adverse pathological effects were noted. Intrathecal nimodipine did not produce a significant dilation of vessels in moderate or severe spasm when assessed by angiography 2 hours after intrathecal injection. Only 1 animal in 8 showed diffuse dilation of vasospastic cerebral vessels after an intrathecal nimodipine injection. Three other animals in this group developed dilation only of the basilar artery, which was in mild spasm.

Animals↗

PubMed1987

Long-term prospective study of lumbosacral discectomy.

A long-term prospective study of 100 patients undergoing lumbosacral discectomy was carried out in an attempt to delineate the natural history of these patients and to assess the relative significance of preoperative factors as determinants of long-term outcome. Neurological findings were documented preoperatively and at 1 month, 1 year, and 5 to 10 years postoperatively. A questionnaire using subjective and objective data was given to patients at 1 year and 5 to 10 years postoperatively. An 83% long-term follow-up result was obtained. At a minimum of 5 years postoperatively, 62% of patients had complete relief of back pain and 62% had complete relief of leg pain; 96% were pleased that they had submitted to surgery and 93% were able to return to work. Nine percent reported that their back pain at 5 to 10 years was as severe as or worse than preoperatively and 11% reported that their leg pain was as severe as or worse than preoperatively. The reoperation rate was 18%. Preoperative factors found to be significantly associated with outcome at 1 year postoperatively were not significantly associated with outcome at 5 to 10 years postoperatively. The results of lumbosacral discectomy appear favorable as evaluated in this study. Preoperative factors useful as predictors of short-term outcome are much less reliable when considering the long-term results.

Adult↗