Avascular necrosis of bone following short-term dexamethasone therapy for brain edema

1984 ◽  
Vol 61 (5) ◽  
pp. 983-985 ◽  
Author(s):  
Avital Fast ◽  
Malvina Alon ◽  
Shmuel Weiss ◽  
Freddy R. Zer-Aviv

✓ The authors present a case of avascular necrosis of both femoral and humeral heads which developed after short-term steroid treatment for brain edema. Avascular necrosis of bone may develop after short-term as well as after maintenance steroid therapy. Early diagnosis with bone scanning and management may in some cases prevent joint destruction.

2000 ◽  
Vol 92 (6) ◽  
pp. 1016-1022 ◽  
Author(s):  
Ya Hua ◽  
Guohua Xi ◽  
Richard F. Keep ◽  
Julian T. Hoff

Object. Brain edema formation following intracerebral hemorrhage (ICH) appears to be partly related to erythrocyte lysis and hemoglobin release. Erythrocyte lysis may be mediated by the complement cascade, which then triggers parenchymal injury. In this study the authors examine whether the complement cascade is activated after ICH and whether inhibition of complement attenuates brain edema around the hematoma.Methods. This study was divided into three parts. In the first part, 100 µl of autologous blood was infused into the rats' right basal ganglia, and the animals were killed at 24 and 72 hours after intracerebral infusion. Their brains were tested for complement factors C9, C3d, and clusterin (a naturally occurring complement inhibitor) by using immunohistochemical analysis. In the second part of the study, the rats were killed at 24 or 72 hours after injection of 100 µl of blood. The C9 and clusterin proteins were quantitated using Western blot analysis. In the third part, the rats received either 100 µl of blood or 100 µl of blood plus 10 µg of N-acetylheparin (a complement activation inhibitor). Then they were killed 24 or 72 hours later for measurement of brain water and ion contents. It was demonstrated on Western blot analysis that there had been a sixfold increase in C9 around the hematoma 24 hours after the infusion of 100 µl of autologous blood. Marked perihematomal C9 immunoreactivity was detected at 72 hours. Clusterin also increased after ICH and was expressed in neurons 72 hours later. The addition of N-acetylheparin significantly reduced brain edema formation in the ipsilateral basal ganglia at 24 hours (78.5 ± 0.5% compared with 81.6 ± 0.8% in control animals, p < 0.001) and at 72 hours (80.9 ± 2.2% compared with 83.6 ± 0.9% in control animals, p < 0.05) after ICH.Conclusions. It was found that ICH causes complement activation in the brain. Activation of complement and the formation of membrane attack complex contributes to brain edema formation after ICH. Blocking the complement cascade could be an important step in the therapy for ICH.


2004 ◽  
Vol 100 (1) ◽  
pp. 2-6 ◽  
Author(s):  
Vaijayantee Kulkarni ◽  
Vedantam Rajshekhar ◽  
Lakshminarayan Raghuram

Object. The authors studied whether cervical spine motion segments adjacent to a fused segment exhibit accelerated degenerative changes on short-term follow-up magnetic resonance (MR) imaging. Methods. Preoperative and short-term follow-up (mean duration 17.5 months, range 10–48 months) cervical MR images obtained in 44 patients who had undergone one- or two-level corpectomy for cervical spondylotic myelopathy were evaluated qualitatively and quantitatively. The motion segment adjacent to the fused segment and a segment remote from the fused segment were evaluated for indentation of the thecal sac, disc height, and sagittal functional diameter of the spinal canal on midsagittal T2-weighted MR images. Thecal sac indentations were classifed as mild, moderate, and severe. New indentations of the thecal sac of varying severity (mild in 17 patients [38.6%], moderate in 10 [22.7%], and severe in six [13.6%]) had developed at the adjacent segments in 33 (75%) of 44 patients. The degenerative changes were seen at the superior level in 11 patients, inferior level in 10 patients, and at both levels in 12 patients and resulted from both anterior and posterior element degeneration in the majority (23 [69.6%]) of patients. The remote segments showed mild thecal sac indentations in seven patients and moderate indentations in two patients (nine [20.5%] of 44). Compared with the changes at the remote segment, the canal size was significantly decreased at the superior adjacent segment by 0.9 mm (p = 0.007). No patient sustained a new neurological deficit due to adjacent-segment changes. Conclusions. On short-term follow-up MR imaging, levels adjacent to the fused segment exhibited more pronounced degenerative changes (compared with remote levels) in 75% of patients who had undergone one- or two-level central corpectomy.


1989 ◽  
Vol 70 (1) ◽  
pp. 73-80 ◽  
Author(s):  
Toshihiko Kuroiwa ◽  
Makoto Shibutani ◽  
Riki Okeda

✓ The effect of suppression of postischemic reactive hyperemia on the blood-brain barrier (BBB) and ischemic brain edema after temporary focal cerebral ischemia was studied in cats under ketamine and alpha-chloralose anesthesia. Regional cerebral blood flow (rCBF) was measured by a thermal diffusion method and a hydrogen clearance method. The animals were separated into three groups. In Group A, the left middle cerebral artery (MCA) was occluded for 6 hours. In Group B, the MCA was occluded for 3 hours and then reperfused for 3 hours; postischemic hyperemia was suppressed to the preischemic level by regulating the degree of MCA constriction. In Group C, the MCA was occluded for 3 hours and reperfused for 3 hours without suppressing the postischemic reactive hyperemia. The brain was removed and cut coronally at the site of rCBF measurement. The degree of ischemic edema was assessed by gravimetry in samples taken from the coronal section and correlated with the degree of BBB disruption at the corresponding sites, evaluated by densitometric determination of Evans blue discoloration. The findings showed that 1) ischemic edema was significantly exacerbated by postischemic hyperemia during reperfusion in parallel with the degree of BBB opening to serum proteins, and 2) suppression of postischemic hyperemia significantly reduced the exacerbation of ischemic edema and BBB opening. These findings indicate that blood flow may be restored without significant exacerbation of postischemic edema by the suppression of postischemic hyperemia in focal cerebral ischemia.


2003 ◽  
Vol 99 (5) ◽  
pp. 863-871 ◽  
Author(s):  
Emad N. Eskandar ◽  
Alice Flaherty ◽  
G. Rees Cosgrove ◽  
Leslie A. Shinobu ◽  
Fred G. Barker

Object. The surgical treatment of Parkinson disease (PD) has undergone a dramatic shift, from stereotactic ablative procedures toward deep brain stimulaion (DBS). The authors studied this process by investigating practice patterns, mortality and morbidity rates, and hospital charges as reflected in the records of a representative sample of US hospitals between 1996 and 2000. Methods. The authors conducted a retrospective cohort study by using the Nationwide Inpatient Sample database; 1761 operations at 71 hospitals were studied. Projected to the US population, there were 1650 inpatient procedures performed for PD per year (pallidotomies, thalamotomies, and DBS), with no significant change in the annual number of procedures during the study period. The in-hospital mortality rate was 0.2%, discharge other than to home was 8.1%, and the rate of neurological complications was 1.8%, with no significant differences between procedures. In multivariate analyses, hospitals with larger annual caseloads had lower mortality rates (p = 0.002) and better outcomes at hospital discharge (p = 0.007). Placement of deep brain stimulators comprised 0% of operations in 1996 and 88% in 2000. Factors predicting placement of these devices in analyses adjusted for year of surgery included younger age, Caucasian race, private insurance, residence in higher-income areas, hospital teaching status, and smaller annual hospital caseload. In multivariate analysis, total hospital charges were 2.2 times higher for DBS (median $36,000 compared with $12,000, p < 0.001), whereas charges were lower at higher-volume hospitals (p < 0.001). Conclusions. Surgical treatment of PD in the US changed significantly between 1996 and 2000. Larger-volume hospitals had superior short-term outcomes and lower charges. Future studies should address long-term functional end points, cost/benefit comparisons, and inequities in access to care.


2005 ◽  
Vol 103 (4) ◽  
pp. 767-768 ◽  
Author(s):  
Zofia Czosnyka ◽  
Marek Czosnyka ◽  
John D. Pickard

Abstract Object. The appearance of numerous B waves during intracranial pressure (ICP) registration in patients with idiopathic adult hydrocephalus syndrome (IAHS) is considered to predict good outcome after shunt surgery. The aim of this study was to describe which physical parameters of the cerebrospinal fluid (CSF) system B-waves reflect and to find a method that could replace long-term B-wave analysis. Methods. Ten patients with IAHS were subjected to long-term registration of ICP and a lumbar constant-pressure infusion test. The B-wave presence, CSF outflow resistance (Rout), and relative pulse pressure coefficient (RPPC) were assessed using computerized analysis. The RPPC was introduced as a parameter reflecting the joint effect of elastance and pulsatory volume changes on ICP and was determined by relating ICP pulse amplitudes to mean ICP. Conclusions. The B-wave presence on ICP registration correlates strongly with RPPC (r = 0.91, p < 0.001, 10 patients) but not with CSF Rout. This correlation indicates that B waves—like RPPC—primarily reflect the ability of the CSF system to reallocate and store liquid rather than absorb it. The RPPC-assessing lumbar short-term CSF pulse pressure method could replace the intracranial long-term B-wave analysis.


1980 ◽  
Vol 52 (4) ◽  
pp. 541-546 ◽  
Author(s):  
Arthur B. Dublin ◽  
William M. Marks ◽  
David Weinstock ◽  
Thomas H. Newton

✓ Three patients with traumatic atlanto-occipital articulation (AOA) dislocation are presented, and an additional 10 well documented cases are reviewed from the literature. Medulla oblongata and/or spinal cord deficits, and evidence of cranial nerve injuries were noted in eight patients. Angiographic evidence of vertebral occlusion or narrowing was demonstrated in four patients. One patient had systemic hypertension, presumably from bilateral traumatic ninth nerve injuries. Five patients ultimately died. A new method for measuring the AOA is introduced.


1971 ◽  
Vol 34 (4) ◽  
pp. 477-487 ◽  
Author(s):  
Robert E. Maxwell ◽  
Don M. Long ◽  
Lyle A. French

✓ Although the beneficial effects of glucosteroids on brain edema are well documented and generally accepted clinically, investigations into their effects on experimental brain edema have been somewhat contradictory. In this study brain edema was produced by local cortical freezing in animals pretreated with glucosteroids and in untreated animals. Gross estimation of edema, wet weight-dry weight determination, and mechanical planimetry of areas of extravasated dye indicated a statistically significant reduction in edema of both white and gray matter at 24, 48, and 72 hours. Gross estimation of edema indicated a persisting effect with resolution of edema at 5 days in treated animals and from 7 to 12 days in untreated animals. These studies substantiate initial investigations and indicate a primary reduction in brain edema by glucosteroids. At least one of the effects of the glucosteroids appears to be reduction of the abnormal vascular permeability causing brain edema.


2000 ◽  
Vol 93 (4) ◽  
pp. 594-604 ◽  
Author(s):  
Michael Bitzer ◽  
Thomas Nägele ◽  
Beverly Geist-Barth ◽  
Uwe Klose ◽  
Eckardt Grönewäller ◽  
...  

Object. In a prospective study, 28 patients with 32 intracranial meningiomas were examined to determine the role of hydrodynamic interaction between tumor and surrounding brain tissue in the pathogenesis of peritumoral brain edema.Methods. Gadolinium—diethylenetriamine pentaacetic acid (Gd-DPTA), an extracellular contrast agent used for routine clinical imaging, remains strictly extracellular without crossing an intact blood—brain barrier. Therefore, it is well suited for investigations of hydrodynamic extracellular mechanisms in the development of brain edema. Spin-echo T1-weighted magnetic resonance images were acquired before and after intravenous administration of 0.2 mmol/kg Gd-DPTA. Additional T1-weighted imaging was performed 0.6, 3.5, and 6.5 hours later. No significant Gd-DPTA diffused from tumor into peritumoral brain tissue in 12 meningiomas without surrounding brain edema. In contrast, in 17 of 20 meningiomas with surrounding edema, contrast agent in peritumoral brain tissue was detectable after 3.5 hours and 6.5 hours. In three of 20 meningiomas with minimum surrounding edema (< 5 cm3), contrast agent effusion was absent. After 3.5 hours and 6.5 hours strong correlations of edema volume and the maximum distance of contrast spread from the tumor margin into adjacent brain parenchyma (r = 0.84 and r = 0.87, respectively, p < 0.0001) indicated faster effusion in larger areas of edema.Conclusions. The results of this study show that significant contrast agent effusion from the extracellular space of the tumor into the interstitium of the peritumoral brain tissue is only found in meningiomas with surrounding edema. This supports the hypothesis that hydrodynamic processes play an essential role in the pathogenesis of peritumoral brain edema in meningiomas.


1998 ◽  
Vol 88 (1) ◽  
pp. 73-76 ◽  
Author(s):  
A. Leland Albright ◽  
Margaret J. Barry ◽  
Michael J. Painter ◽  
Barbara Shultz

Generalized dystonia occurs in 15 to 25% of persons with cerebral palsy (CP) and responds poorly to medical and surgical treatments. Object. After the authors observed a woman whose dystonic CP was dramatically improved by continuous infusion of intrathecal baclofen, they designed this pilot study to evaluate the effect of this treatment on a group of patients with dystonic CP. Methods. The authors assessed the short-term response to intrathecal baclofen infusion in 12 patients with dystonic CP. An intrathecal catheter was inserted percutaneously and connected to an external microinfusion pump. The infusion began at a rate of 100 µg/day and was increased by 50 µg every 12 hours until the dystonia abated, adverse effects occurred, or the dose reached 900 mg/day with no improvement. Two observers, one blinded and one not blinded to the patient's treatment status, viewed videotapes made before and after the infusions and graded the dystonia in eight body regions, using a 5-point scale. Overall and regional scores were compared by using Wilcoxon signed-rank tests. Conclusions. Dystonia diminished in 10 of 12 patients whose average daily dose of intrathecal baclofen was 575 µg. Overall dystonia scores and scores for the extremities, trunk, and cervical regions were significantly better after infusion (p = 0.003). The two observers' scores were not significantly different. Programmable infusion pumps were subsequently implanted in eight patients for long-term therapy and improvement was sustained in six (p < 0.05). Intrathecal baclofen infusion is a promising treatment option for generalized dystonia associated with CP. The effects of intrathecal baclofen infusion on dystonia can be evaluated by using short-term continuous infusions.


1985 ◽  
Vol 63 (6) ◽  
pp. 830-839 ◽  
Author(s):  
Eiji Yoshino ◽  
Tarumi Yamaki ◽  
Toshihiro Higuchi ◽  
Yoshiharu Horikawa ◽  
Kimiyoshi Hirakawa

✓ Dynamic computerized tomography (CT) was performed on 42 patients with acute head injury to evaluate the hemodynamics and to elucidate the nature of fatal diffuse brain bulk enlargement. Patients were divided into two groups according to the outcome: Group A included 17 nonfatally injured patients, eight with acute epidural hematomas and nine with acute subdural hematomas; Group B included 25 fatally injured patients, 16 with acute subdural hematomas and nine with bilateral brain bulk enlargement. Remarkable brain bulk enlargement could be seen in all fatally injured patients with acute subdural hematoma. In 29 (69%) of 42 patients, dynamic CT was performed within 2 hours after the impact. In the nonfatally injured patients with brain bulk enlargement, dynamic CT scans suggested a hyperemic state. On the other hand, in 17 (68%) of the 25 fatally injured patients, dynamic CT scans revealed a severely ischemic state. In the fatally injured patients with acute subdural hematoma, CT Hounsfield numbers in the enlarged hemisphere (hematoma side) were significantly lower than those of the opposite side (p < 0.001). Severe diffuse brain damage confirmed by follow-up CT scans and uncontrollable high intracranial pressure were noted in the fatally injured patients. Brain bulk enlargement following head injury originates from acute brain edema and an increase of cerebral blood volume. In cases of fatal head injury, acute brain edema is the more common cause of brain bulk enlargement and occurs more rapidly than is usually thought.


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