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A new "gamma-extension" device for the Brown-Roberts-Wells arc system allowing full lateral stereotactic approaches
No full textA pair of clamps for a safe removing and repositioning of beta and gamma angular settings of Brown-Roberts-Wells stereotactic system during operation
No full textThe Brown-Roberts-Wells are system is a non-target-centered design, i.e., without an independent approach angle. The approach angle of this system strictly depends on precalculated values (entry and target point). Therefore, some components of the system used sometimes prevent a direct insight into the operation field. Once the entry point has been set, the are system normally has to be taken off to permit an unimpeded approach to the burr here. To facilitate rotation and return to the primary beta and gamma angular settings during stereotactic craniotomy and other surgery, a pair of clamps was designed for the BRW are system. These clamps help the approach to the entry point in such a way that some components of the are (e.g., the guide block holder) are removed from the surgical field, thus giving wide visual access for the stereotactic approach. Consequently, it is no longer necessary to remove the entire are system, resulting in an increased operation safety and shorter operation times
Expression of nitric oxide synthase isozymes (NOS I-III) by immunohistochemistry and DNA in situ hybridization. Correlation with macrophage presence, vascular endothelial growth factor (VEGF) and oedema volumetric data in 220 glioblastomas
No full textBackground: Nitric oxide (NO) is synthesized from arginine by three different isozymes of nitric oxide synthase (NOS I-III). NO has been identified as a powerful metabolite cf vascular smooth muscle cell function, cerebral blood circulation and oedema induction. NOS induction by different cytokines has been shown previously in glioblastoma cell cultures and NOS III expression due to astrocytoma grading has been shown in several tumors recently. The aim of the present study was to study the coexpression of NOS I-III, macrophage and capillary presence with VEGF, ECF and their receptors and to investigate a possible mechanism in peritumoral oedema generation.. Materials and Methods: We have investigated the expression (4- grade values, blinded assay by two observers) of NOS I-III together with those of VEGF, VEGF-R (Flt-1), EGF-R1, von-Willebrand-factor (VWF) and a pan-macrophage marker (ki-MIP) immunohistochemically in tumor specimens from 220 patients and performed tumor volume morphometry by image analysis in a subgroup of 32 cases to test for any correlation with the peritumoral oedema volumes. Inducible NOS II was further investigated by in situ labelling with a DNA oligonucleotide probe cocktail. Results: All of the specimens revealed some NOS expression, NOS II was expressed in macrophages, microglia and endothelial cells, NOS III and I was localized in glioblastoma cells, NOS III in endothelial cells as well. The highest degrees of expression were observed in 46% (NOS I), 22% (NOS II) and 75% (NOS III) of all specimens, Inducible NOS II in any expression grade was observed in 47.5% of the specimens. Significant correlations were observed for the expression of the macrophage marker Ki-M1P with NOS II (p = 0.024), endothelial NOS III with NOS I (p = 00003), VEGF-R1 with NOS II (p = 0.0008) and NOS III (p = 0.011) The oedema volumes could not be correlated significantly with NOS or VEGF-R1 expression values but with those of endothelial staining (p = 002). We observed a trend towards higher Ki-MIP expression values together with higher oedema volume extensions. In situ hybridization demonstrated reaction products in endothelial and perivascular regions and sometimes scattered throughout the specimens revealing the labelling of macrophages. Conclusions: The main source of NO is NOS I and NOS III The latter is located in endothelial cells and glioblastoma cells. The expression of NOS II in glioblastomas is restricted to infiltrating macrophages. NOS II and III expressions were observed significantly together with that of VEGF-R1. Neither NOS I-III nor VEGF-R expression could be correlated with the extension of the peritumoral oedema
Expression of nitric oxide synthase isozymes (NOS I-III) by immunohistochemistry and DNA in situ hybridization. Correlation with macrophage presence, vascular endothelial growth factor (VEGF) and oedema volumetric data in 220 glioblastomas
No full textBackground: Nitric oxide (NO) is synthesized from arginine by three different isozymes of nitric oxide synthase (NOS I-III). NO has been identified as a powerful metabolite cf vascular smooth muscle cell function, cerebral blood circulation and oedema induction. NOS induction by different cytokines has been shown previously in glioblastoma cell cultures and NOS III expression due to astrocytoma grading has been shown in several tumors recently. The aim of the present study was to study the coexpression of NOS I-III, macrophage and capillary presence with VEGF, ECF and their receptors and to investigate a possible mechanism in peritumoral oedema generation.. Materials and Methods: We have investigated the expression (4- grade values, blinded assay by two observers) of NOS I-III together with those of VEGF, VEGF-R (Flt-1), EGF-R1, von-Willebrand-factor (VWF) and a pan-macrophage marker (ki-MIP) immunohistochemically in tumor specimens from 220 patients and performed tumor volume morphometry by image analysis in a subgroup of 32 cases to test for any correlation with the peritumoral oedema volumes. Inducible NOS II was further investigated by in situ labelling with a DNA oligonucleotide probe cocktail. Results: All of the specimens revealed some NOS expression, NOS II was expressed in macrophages, microglia and endothelial cells, NOS III and I was localized in glioblastoma cells, NOS III in endothelial cells as well. The highest degrees of expression were observed in 46% (NOS I), 22% (NOS II) and 75% (NOS III) of all specimens, Inducible NOS II in any expression grade was observed in 47.5% of the specimens. Significant correlations were observed for the expression of the macrophage marker Ki-M1P with NOS II (p = 0.024), endothelial NOS III with NOS I (p = 00003), VEGF-R1 with NOS II (p = 0.0008) and NOS III (p = 0.011) The oedema volumes could not be correlated significantly with NOS or VEGF-R1 expression values but with those of endothelial staining (p = 002). We observed a trend towards higher Ki-MIP expression values together with higher oedema volume extensions. In situ hybridization demonstrated reaction products in endothelial and perivascular regions and sometimes scattered throughout the specimens revealing the labelling of macrophages. Conclusions: The main source of NO is NOS I and NOS III The latter is located in endothelial cells and glioblastoma cells. The expression of NOS II in glioblastomas is restricted to infiltrating macrophages. NOS II and III expressions were observed significantly together with that of VEGF-R1. Neither NOS I-III nor VEGF-R expression could be correlated with the extension of the peritumoral oedema
Expression of focal adhesion kinase (p125 FAK) and proline-rich tyrosine kinase 2 (PYK2/CAKb) in cerebral metastases, correlation with VEGF-R-, ecNOS III-labelling and morphometric data
No full textBackground: Cerebral metastasis occurs in about 20% of all neurosurgical patients. Cerebral metastases have a typical spherical morphology with a common central necrosis and perifocal oedema. It has been proposed that oedema extension, tumour volumes and infiltrative behaviour are partially mediated by vascular endothelial growth factor (VEGF) and nitric oxide (NO). In several systemic tumour entities NO is suggested as a factor which influences the metastatic potential VEGF has recently been reported to influence the matrix related migratory activity by interaction with focal adhesion kinase (p125FAK) and proline-rich tyrosine kinase beta (PYK2/CAK beta). Nitric oxide, which is produced in metastases by three different NOS isozymes is capable of antagonizing the binding of FAK to matrix integrins. NO, VEGF; and FAK/PYK 2 are therefore considered to be important mediators of the cerebral metastatic incidence, growth, infiltration and oedema extension. The aim of our present study was to investigate the expression of p125FAK and the coexpression with PYK2/CAK beta, VEGF-receptor FLT-1, NOS isozymes NOS I-III, capillary density and the histology in 130 specimens of resected cerebral metastatic tumours. A further analysis was performed to morphometrically evaluate tumour and oedema volumes and to correlate the immunohistochemical data. in a subgroup of 40 patients. Materials and methods: Cryosections (N = 130) of metastatic resections were investigated immunohistologically using a 4-step scoring evaluation for the expression of NOS I-III, VEGF-receptor FLT-1, and capillary vessel presence by endothelial Von-Willebrand-Factor (VWF) staining. Tumour and oedema extension was measured in preoperative MRI (N = 40) scans by an imageo processing device (Kontron(R)) and the ratios of oedema volumes to total tumour volumes were calculated The data were analysed statistically (Spearman rank order con elation and Kruskal-Wallis ANOVA) and con-elated with the clinical data. Results: FAK immunoexpression was observed in 50% of the specimens (31.2% gradings 2 and 3). We observed a significant coexpression (p = 0.0001) with PYK 2 labelling which occurred frequently in 74% of the specimens (42% gradings 2 and 3). The VEGF receptor FLT-1 could be detected in 70% of them, 24% at higher expression values 2 and 3. The expression of NO synthase was frequently observed. NOS I was detected in 83.6% of the specimens, values 2 and 3 in 40.5%. NOS III, the endothelial isoform, was observed in 39.4% of the specimens (gradings 2 and 3) and inducible NOS II in 29.4% (grading 2 and 3) of them. Coexpressions were statistically significant for FAK and NOS III (Spearman p = 0.008) and FAK and VEGF-R (p = 0.03). The morphometric evaluation resulted in tumour volumes between 2.0 and 83 cm(3) (mean 22.5 +/- 19.2 SD) with oedema ratios between 0 and 100% (mean 62.2 +/- 22.5 SD). FAK expression correlated significantly (p = 0.06) with tumour. volumes and histology. Conclusion: The frequent histotypic occurence of FAK and PYK2 in metastases could be an important factor in the modulation of metastatic capacity and infiltrative behaviour and might influence the disease course. Judging from its frequent expression PYK2 may generate the more relevant signals. A further aspect is the possible interaction with endothelial NOS III and VEGF receptor; which could be important for the infiltrative behaviour in a Intent hypoxic scenery and environment
Improved visibility of the subthalamic nucleus on high-resolution stereotactic MR imaging by added susceptibility (T2*) contrast using multiple gradient echoes
No full textReliable identification of the subthalamic nucleus (STN) is a critical step in deep brain stimulation for Parkinson disease but difficult on TI-weighted stereotactic MR imaging. By simultaneous imaging of multiple gradient echoes, susceptibility contrast is added to conventional T1weighted high-resolution MR image. Thus, the visibility of the STN is enhanced on a second colocalized dataset by exploiting the sensitivity of the T2 -relaxation to local iron deposits. The feasibility is underpinned by quantitative measurements on healthy adults
Intraosseous Ultrasound in the Placement of Pedicle Screws in the Lumbar Spine
No full textStudy Design. Experimental and intraoperative evaluation of the efficiency of a novel technique. Objective. To determine the accuracy of pedicle screw hole placements before screw implantation in the lumbar spine. Summary of Background Data. Deviations from planned trajectories occur in a significant number of screw placements in posterior lumbar fixation. Several techniques have been proposed to minimize this complication, although none has gained general acceptance. This may be due to costs associated with their implementation or considerably extended operating times required by some techniques. Methods. Pedicle screw holes were placed in 24 pedicles of 2 postmortem human lumbar spine specimens. Sixteen optimal trajectories were placed and 8 intentional cortical breaches. Each pedicular drill hole was examined using a 360 ultrasound transducer and CT scanning. The ultrasonographic images were reviewed by 3 independent investigators who were blinded to the CT findings. In addition, 20 screw holes were placed intraoperatively in 3 patients, and equally assessed by intraoperative intraosseous ultrasonography and postoperative CT scanning. Results. Ultrasonographic images of pedicle screw holes in postmortem human spine specimen were correctly interpreted in 99% of cases. No cortical breech was missed, i.e., no false-negatives occurred. Intraoperative findings closely matched the experimental data. None of the intraoperative ultrasound scans demonstrated a cortical breach, a finding confirmed by postoperative CT. The intraoperative time required for the ultrasonographic analysis of each pedicle was about 1 minute and the interpretation of the resulting images was judged intuitive by the evaluating neurosurgeons. Conclusion. Intraosseous ultrasound is a highly reliable technique for the intraoperative assessment of pedicle screw holes before pedicle screw placement. Additional expenses with respect to procedure time and manpower are minimal
Expression of focal adhesion kinase (p125 FAK) and proline-rich tyrosine kinase 2 (PYK2/CAKb) in cerebral metastases, correlation with VEGF-R-, ecNOS III-labelling and morphometric data
No full textBackground: Cerebral metastasis occurs in about 20% of all neurosurgical patients. Cerebral metastases have a typical spherical morphology with a common central necrosis and perifocal oedema. It has been proposed that oedema extension, tumour volumes and infiltrative behaviour are partially mediated by vascular endothelial growth factor (VEGF) and nitric oxide (NO). In several systemic tumour entities NO is suggested as a factor which influences the metastatic potential VEGF has recently been reported to influence the matrix related migratory activity by interaction with focal adhesion kinase (p125FAK) and proline-rich tyrosine kinase beta (PYK2/CAK beta). Nitric oxide, which is produced in metastases by three different NOS isozymes is capable of antagonizing the binding of FAK to matrix integrins. NO, VEGF; and FAK/PYK 2 are therefore considered to be important mediators of the cerebral metastatic incidence, growth, infiltration and oedema extension. The aim of our present study was to investigate the expression of p125FAK and the coexpression with PYK2/CAK beta, VEGF-receptor FLT-1, NOS isozymes NOS I-III, capillary density and the histology in 130 specimens of resected cerebral metastatic tumours. A further analysis was performed to morphometrically evaluate tumour and oedema volumes and to correlate the immunohistochemical data. in a subgroup of 40 patients. Materials and methods: Cryosections (N = 130) of metastatic resections were investigated immunohistologically using a 4-step scoring evaluation for the expression of NOS I-III, VEGF-receptor FLT-1, and capillary vessel presence by endothelial Von-Willebrand-Factor (VWF) staining. Tumour and oedema extension was measured in preoperative MRI (N = 40) scans by an imageo processing device (Kontron(R)) and the ratios of oedema volumes to total tumour volumes were calculated The data were analysed statistically (Spearman rank order con elation and Kruskal-Wallis ANOVA) and con-elated with the clinical data. Results: FAK immunoexpression was observed in 50% of the specimens (31.2% gradings 2 and 3). We observed a significant coexpression (p = 0.0001) with PYK 2 labelling which occurred frequently in 74% of the specimens (42% gradings 2 and 3). The VEGF receptor FLT-1 could be detected in 70% of them, 24% at higher expression values 2 and 3. The expression of NO synthase was frequently observed. NOS I was detected in 83.6% of the specimens, values 2 and 3 in 40.5%. NOS III, the endothelial isoform, was observed in 39.4% of the specimens (gradings 2 and 3) and inducible NOS II in 29.4% (grading 2 and 3) of them. Coexpressions were statistically significant for FAK and NOS III (Spearman p = 0.008) and FAK and VEGF-R (p = 0.03). The morphometric evaluation resulted in tumour volumes between 2.0 and 83 cm(3) (mean 22.5 +/- 19.2 SD) with oedema ratios between 0 and 100% (mean 62.2 +/- 22.5 SD). FAK expression correlated significantly (p = 0.06) with tumour. volumes and histology. Conclusion: The frequent histotypic occurence of FAK and PYK2 in metastases could be an important factor in the modulation of metastatic capacity and infiltrative behaviour and might influence the disease course. Judging from its frequent expression PYK2 may generate the more relevant signals. A further aspect is the possible interaction with endothelial NOS III and VEGF receptor; which could be important for the infiltrative behaviour in a Intent hypoxic scenery and environment
Oedema extension in cerebral metastasis and correlation with the expression of nitric oxide synthase isozymes (NOS I-III)
No full textBackground: The development of a peritumoral oedema is a common radiological sign in preoperative CT- and MRI scans of patients with cerebral metastasis. Large tumours can be accompanied by a marginally extended oedema and vice versa. Several cytokines (VEGF) have been identified as mediators of vascular induction and permeability. Transmitters such as nitric oxide (NO) have been identified as specific mediator of vascular dilation and tumour blood flow in primary brain tumours in which different NOS isozymes (NOS I and III) are induced as a result of the latent hypoxic metabolic scenery Other authors have considered NO as an endothelial stabilising metabolite. Inducible NOS II is expressed by microglia and macrophages invading during tumour growth. At present, no data exist on NO synthesising enzymes in cerebral metastasis. Materials and Patients: Cryosections (N = 96) of metastatic resections were investigated immunohistologically using a 4-step grading evaluation for the expression of NOS I-III VEGF-receptor FLT-1, a pan-macrophage marker Ki-M1P, and capillary vessel presence by endothelial Ki-Willebrand-Factor staining. The tumour and oedema extension was measured in pre MRI scans by an image processing device (Kontron(R)) and calculated for the ratios of oedema volumes to total tumour volumes. The data were analysed statistically (Pearson Chi(2) and Kruskal-Wallis analysis of variances) and correlated with the clinical data. Inducible NOS II was further investigated by in situ hybridization with a (4x30 mer) DNA oligoprobe cocktail Results: Between 1987 and 1996 289 patients in our department suffered from a metastatic disease in the brain or spinal cord In 96 cases resected tumour material was processed for the immunohistological investigation. The age distribution ranged from 14 to 85 years with a median age of 58 years. The mean duration of symptoms before diagnosis was estimated as 53 days. The expression of NO synthase was frequently observed NOS I was detected in 83.6%, gradings 2 and 3 in 40.5% of them. NOS III, the endothelial isoform, was observed in 39.4% (gradings 2 and 3), inducible NOS II in 29.4% (grading 2 and 3) of the specimens. The VEGF receptor FLT-I could be detected in 70% of them, 24% in higher expression 2 and 3. The pan macrophage marker Ki-MIP was observed in 72% of all cases. Fifty seven percent of the specimens exhibited strong labelling with antibodies against VWF. Coexpressions were statistically significant for the VEGF receptor and NOS I-III (p < 0.01), Ki-M1P and NOS I and II (p < 0.05). A negative correlation was detected for the oedema index (oedema volume/total volume) and the labelling data for NOS III (r =- 0.44, p = 0.13) and VEGF-R (r = -0.42, p = 0.022). No correlation existed for Ki-MIP, VWF and NOS I. Conclusions: The objective of the study was to investigate oedema morphometry, expression of NOS I-III and VEGF-R, presence of capillary vessels and macrophages in cerebral metastasis. A further aim was to investigate a putative oedema induction by NO producing isozymes. Nitric oxide synthase expression was statistically significantly correlated with the expression of the VEGF receptor and the presence of macrophages and microglia. There was a negative correlation between oedema extension and the presence of NOS III and VEGF-R. The results seem to indicate a specific oedema modulating role of NO in cerebral metastasis
Intraosseous ultrasonography to determine the accuracy of drill hole positioning prior to the placement of pedicle screws: an experimental study
No full text
Object
Dorsal fixation with rods and pedicle screws (PSs) is the most frequently used surgery to correct traumatic and degenerative instabilities of the human spine. Prior to screw placement, screw holes are drilled along the vertebral pedicles. Despite the use of a variety of techniques, misplacement of screw holes, and consequently of the PSs, is a common problem. The authors investigated the usefulness of an intraspinal, intraosseous ultrasonography technique to determine the accuracy of drill hole positioning.
Methods
An endovascular ultrasound transducer was used for the intraluminal scanning of bore holes in trabecular bovine bone, 12 pedicle drill holes in cadaveric human spine, and 4 pedicle drill holes in a patient undergoing thoracic spondylodesis. Seven of the experimental bore holes in the cadaveric spine were placed optimally (that is, inside the pedicle) and 5 were placed suboptimally (breaching the medial or lateral cortical surface of the pedicle). Computed tomography scans were obtained in the patient and cadaveric specimen after the procedure.
Results
The image quality achieved in examinations of native bovine bone tissue, the formalin-fixed human spine specimen, and human vertebrae in vivo was equal. The authors endosonographically identified correct intrapedicular and intravertebral positions as well as poor (cortex breached) placement of drill holes.
Conclusions
Intraosseous ultrasonography is a promising technique for the investigation of PS holes prior to screw implantation, and may add to the safety of PS placement.</jats:sec
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