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F Schmidt

Publications and source records attributed to F Schmidt.

At least 73 records · Page 4Linked to original sources

Evidence for a melatonin receptor within pancreatic islets of neonate rats: functional, autoradiographic, and molecular investigations.

In a recent perifusion investigation, we showed that the pineal secretory product melatonin reduces insulin secretion from isolated pancreatic islets of neonate rats stimulated with potassium chloride (KCl), glucose, and forskolin. This effect of melatonin was reproduced with doses ranging from 200 pmol/L to 5 micromol/L. Because it is generally accepted that melatonin exerts some of its biological effects through specific, high-affinity pertussis-toxin-sensitive G-protein-coupled receptors, we blocked the putative melatonin receptor of pancreatic islets using both the non-hydrolyzable guanosine triphosphate analog guanosine 5'-O-(3-thiotriphosphate) (GTPgammaS, 30 micromol/L) and the melatonin antagonist luzindole (10 micromol/L). Both GTPgammaS and luzindole caused a near normalization of the melatonin-induced inhibition of the forskolin-stimulated insulin secretion. To localize putative melatonin receptors within the pancreatic islets autoradiographic studies were additionally carried out. These investigations showed specific binding of 2-[125I]iodomelatonin, which were in exact correspondence with the localization of the islets. In addition, gray-level analysis showed that unlabeled melatonin was able to reduce the binding of 2-[125I]iodomelatonin in a dose-dependent manner. Concentrations of unlabeled melatonin of 10(-9) mol/L produced a 50% reduction in specific binding, whereas concentrations of 10(-6) mol/L displaced the binding completely. Likewise, the results of molecular investigations showed that the rat pancreas contains a melatonin receptor, since reverse transcription polymerase chain reaction (RT-PCR) experiments, using specific primers for the rat melatonin receptor Mel1a, showed that mRNA for this melatonin receptor type is expressed in pancreatic tissue of newborn rats. In summary, it may be said that our functional. autoradiographic, and molecular results indicate that the Mel1a receptor is located on the pancreatic islets, possibly in the beta cells.

Animals↗

Gender specificity of tolterodine on micturition and the diurnal variation of urine production of the conscious rat.

OBJECTIVE: To evaluate the effect of the oral administration of tolterodine on the diurnal micturition characteristics of the male and female conscious rat, and to examine the relative effect of tolterodine in influencing water consumption and urine production. MATERIALS AND METHODS: Baseline micturition volume and frequency characteristics of nine male and 10 female Sprague-Dawley age-matched adult rats (body weight 399 +/- 15 and 249 +/- 3 g, respectively) were evaluated over 24-h. Initial hydration conditions were standardized with an oral dose (5 mL) of water. Rats were subsequently placed in a metabolic cage and had free access to water. Micturition volume/frequency characteristics were derived from the measurements of voided volume (measured using a digital balance below the metabolic cage and connected to a computer). The total volume of water consumed over the 24 h was also measured. Two separate baseline studies were conducted, followed by the administration of a single oral dose of 1 mg/mL of tolterodine dissolved in 5 mL of water. The mean frequency of micturition and mean volume voided per micturition were computed in 3-h periods and plotted over the 24-h period. In addition, the mean values of the number of micturitions and voided volumes during the day/dark cycle were evaluated. RESULTS: Baseline data showed that females (when corrected for body weight) consistently imbibed significantly more water (83%) than did male rats. Tolterodine did not significantly affect water consumption in the males but significantly reduced water consumption in females by 42%. Tolterodine did not significantly affect the amount of urine produced by male rats but significantly reduced the total amount of urine production in females by 26%. Tolterodine significantly increased the number of voids in male rats compared with baseline during the day but not during the night. More importantly tolterodine produce no significant effect on the volume voided per micturition in male rats either during the day or night cycle, but significantly decreased the volume voided per micturition in females. CONCLUSIONS: These results suggest that the effect of tolterodine on micturition is gender-specific, suppressing water consumption and urine production in female but not male rats, and decreasing bladder volume. There is a possibility that the reported clinical effects of tolterodine arise through the suppression of fluid consumption.

Animals↗

Cerivastatin prevents angiotensin II-induced renal injury independent of blood pressure- and cholesterol-lowering effects.

BACKGROUND: Statins are effective in prevention of end-organ damage; however, the benefits cannot be fully explained on the basis of cholesterol reduction. We used an angiotensin II (Ang II)-dependent model to test the hypothesis that cerivastatin prevents leukocyte adhesion and infiltration, induction of inducible nitric oxide synthase (iNOS), and ameliorates end-organ damage. METHODS: We analyzed intracellular targets, such as mitogen-activated protein kinase and transcription factor (nuclear factor-kappaB and activator protein-1) activation. We used immunohistochemistry, immunocytochemistry, electrophoretic mobility shift assays, and enzyme-linked immunosorbent assay techniques. We treated rats transgenic for human renin and angiotensinogen (dTGR) chronically from week 4 to 7 with cerivastatin (0.5 mg/kg by gavage). RESULTS: Untreated dTGR developed hypertension, cardiac hypertrophy, and renal damage, with a 100-fold increased albuminuria and focal cortical necrosis. dTGR mortality at the age of seven weeks was 45%. Immunohistochemistry showed increased iNOS expression in the endothelium and media of small vessels, infiltrating cells, afferent arterioles, and glomeruli of dTGR, which was greater in cortex than medulla. Phosphorylated extracellular signal regulated kinase (p-ERK) was increased in dTGR; nuclear factor-kappaB and activator protein-1 were both activated. Cerivastatin decreased systolic blood pressure compared with untreated dTGR (147 +/- 14 vs. 201 +/- 6 mm Hg, P < 0.001). Albuminuria was reduced by 60% (P = 0.001), and creatinine was lowered (0.45 +/- 0.01 vs. 0.68 +/- 0.05 mg/dL, P = 0. 003); however, cholesterol was not reduced. Intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression was diminished, while neutrophil and monocyte infiltration in the kidney was markedly reduced. ERK phosphorylation and transcription factor activation were reduced. In addition, in vitro incubation of vascular smooth muscle cells with cerivastatin (0.5 micromol/L) almost completely prevented the Ang II-induced ERK phosphorylation. CONCLUSION: Cerivastatin reduced inflammation, cell proliferation, and iNOS induction, which led to a reduction in cellular damage. Our findings suggest that 3-hydroxy-3-methylglutaryl coenzyme (HMG-CoA) reductase inhibition ameliorates Ang II-induced end-organ damage. We suggest that these effects were independent of cholesterol.

Albuminuria↗

Human malignant glioma cell lines are refractory to retinoic acid-mediated differentiation and sensitization to apoptosis.

BACKGROUND: Retinoids are candidate differentiation-inducing agents for glial tumors. Differentiation therapy is an attractive approach to cancers that resist surgery, irradiation and chemotherapy. METHODS: We examined the effects of retinoids on proliferation, morphology and sensitivity to apoptosis in human malignant glioma and neuroblastoma cell lines. RESULTS: In contrast to neuroblastoma cells, retinoids are devoid of acute cytotoxic effects and have only moderate antiproliferative effects on human glioma cell lines upon long-term exposure at high concentrations. Electron microscopy fails to reveal features of differentiation or apoptosis in retinoid-treated glioma cells and untransformed rat astrocytes. Retinoids do not modulate CD95 or CD95L expression or susceptibility to CD95-mediated apoptosis and fail to act in synergy with interferon (IFN)-alpha or IFN-gamma or cancer chemotherapy drugs to promote growth inhibition or apoptosis. CONCLUSION: Glioma cell lines are refractory to the induction of differentiation or apoptosis by retinoids.

Animals↗

Adding low-dose antidepressants to interferon alpha treatment for chronic hepatitis C improved psychiatric tolerability in a patient with schizoaffective psychosis.

Treatment of chronic hepatitis C with interferon alpha (IFN-alpha) is relatively contraindicated in patients with psychiatric disorders because of possible severe psychiatric side effects. We report on a case of a female patient with a chronic schizoaffective psychosis, who was treated for 3 months with 3 x 3 mio IE IFN-alpha s.c./week because of a chronic hepatitis C (genotype 1b). Psychosis was stable with flupentixol monotherapy. After 2 months, she developed a severe depressive syndrome which lead to suicidal ideation. Until this time, she was without any antidepressive medication. Depressive symptoms disappeared after interferon therapy was stopped. Under prophylactic treatment with low-dose trimipramine (50 mg) or nefazodone (200 mg/day) therapy with IFN-alpha 3 x 3 mio IE/week was re-established after several months and again 2 years later adding ribavirin 1200 mg/day, a virustaticum. In contrast to the symptoms during monotherapy with IFN-alpha, during the time of both combination treatments, no psychiatric side effects occurred. While for ribavirin antidepressant effects are not known, we suppose that antidepressants may prevent changes in serotonergic or noradrenergic neurotransmission caused by IFN-alpha.

Adult↗

NF-kappaB inhibition ameliorates angiotensin II-induced inflammatory damage in rats.

We recently reported that the activation of nuclear factor-kappaB (NF-kappaB) promotes inflammation in rats harboring both human renin and angiotensinogen genes (double-transgenic rats [dTGR]). We tested the hypothesis that the antioxidant pyrrolidine dithiocarbamate (PDTC) inhibits NF-kappaB and ameliorates renal and cardiac end-organ damage. dTGR feature hypertension, severe renal and cardiac damage, and a 40% mortality rate at 7 weeks. Electrophoretic mobility shift assay showed increased NF-kappaB DNA binding activity in hearts and kidneys of dTGR. Chronic PDTC (200 mg/kg SC) treatment decreased blood pressure (162+/-8 versus 190+/-7 mm Hg; P=0.02) in dTGR compared with dTGR controls. The cardiac hypertrophy index was also significantly reduced (4.90+/-0.1 versus 5.77+/-0.1 mg/g; P<0. 001). PDTC reduced 24-hour albuminuria by >95% (2.5+/-0.8 versus 57. 1+/-8.7 mg/d; P<0.001) and prevented death. Vascular injury was ameliorated in small renal and cardiac vessels. Electrophoretic mobility shift assay showed that PDTC inhibited NF-kappaB binding activity in heart and kidney, whereas AP-1 activity in the kidney was not decreased. dTGR exhibited increased left ventricular c-fos and c-jun mRNA expression. PDTC treatment reduced c-fos but not c-jun mRNA. Immunohistochemistry showed increased p65 NF-kappaB subunit expression in the endothelium and smooth muscle cells of damaged small vessels, as well as infiltrating cells in glomeruli, tubules, and collecting ducts of dTGR. PDTC markedly reduced the immunoreactivity of p65. PDTC also prevented the NF-kappaB-dependent transactivation of the intercellular adhesion molecule ICAM-1 and inducible nitric oxide synthase. Monocyte infiltration was markedly increased in dTGR kidneys and hearts. Chronic treatment reduced monocyte/macrophage infiltration by 72% and 64%, respectively. Thus, these results demonstrate that PDTC inhibits NF-kappaB activity, ameliorates inflammation, and protects against angiotensin II-induced end-organ damage.

Angiotensin II↗

Cyclosporin A protects against angiotensin II-induced end-organ damage in double transgenic rats harboring human renin and angiotensinogen genes.

Leukocyte infiltration and adhesion molecule activation play a central role in the pathogenesis of angiotensin II (Ang II)-induced end-organ damage in double transgenic rats (dTGR) harboring human renin and angiotensinogen genes. We tested the hypothesis that the immunosuppressive agent cyclosporine (CsA) protects against the Ang II-induced myocardial and renal damage in dTGR. Furthermore, we investigated the influence of CsA on interleukin-6 (IL-6) and inducible nitric oxide synthase (iNOS) expression and the DNA binding activity of transcription factor necrosis factor-kappaB (NF-kappaB). The 4-week-old rats were divided into 4 groups: (1) control dTGR (n=20), (2) dTGR plus CsA (5 mg/kg SC for 3 weeks, n=15), (3) normotensive Sprague-Dawley (SD) rats (n=10), and (4) SD rats plus CsA (n=8). In dTGR, CsA completely prevented cardiovascular death (0 of 15 versus 9 of 20), decreased 24-hour albuminuria by 90% and systolic blood pressure by 35 mm Hg, and protected against the development of cardiac hypertrophy. Whole blood CsA concentrations 24 hours after the last drug treatment were 850+/-15 ng/mL. Semiquantitative ED-1 and Ki-67 (a nuclear cell proliferation-associated antigen) scoring showed that CsA prevented perivascular monocyte/macrophage infiltration and prevented cell proliferation in the kidneys and hearts of dTGR, respectively. The beneficial effects of CsA were, at least in part, mediated by the suppression of IL-6 and iNOS expression. Electrophoretic mobility shift assay revealed that CsA regulated inflammatory response in part through the NF-kappaB transcriptional pathway. In contrast to dTGR, CsA increased blood pressure in normotensive SD rats by 10 mm Hg and had no effect on cardiac mass or 24-hour urinary albumin excretion. Perivascular monocyte/macrophage infiltration, IL-6, and iNOS expression or cell proliferation were not affected by CsA in SD rats. Our findings indicate that CsA protects against Ang II-induced end-organ damage and underscore the central role of vascular inflammatory response in the pathogenesis of myocardial and renal damage in dTGR. The beneficial effects of CsA in the kidney and heart are mediated, at least in part, by suppression of IL-6 and iNOS expression via NF-kappaB transcriptional pathway.

Albuminuria↗

Blood pressure-independent effects in rats with human renin and angiotensinogen genes.

The blood pressure-independent effects of angiotensin II (Ang II) were examined in double transgenic rats (dTGR) harboring human renin and human angiotensinogen genes, in which the end-organ damage is due to the human components of the renin angiotensin system. Triple-drug therapy (hydralazine 80 mg/L, reserpine 5 mg/L, and hydrochlorothiazide 25 mg/L in drinking water) was started immediately after weaning. Triple-drug therapy normalized blood pressure and coronary resistance, only partially prevented cardiac hypertrophy, and had no effect on ratio of renal weight to body weight. Although triple-drug therapy delayed the onset of renal damage, severe albuminuria nevertheless occurred. Semiquantitative scoring of ED-1-positive and MIB-5-positive (nuclear cell proliferation-associated antigen Ki-67) cells showed profound perivascular monocyte/macrophage infiltration and cell proliferation in kidneys and hearts of untreated dTGR. Triple-drug therapy had only a minimal effect on local inflammatory response or vascular cell proliferation. In contrast, a novel orally active human renin inhibitor (HRI), 30 mg/kg by gavage for 4 weeks, normalized blood pressure and coronary resistance and also prevented cardiac hypertrophy and albuminuria. ED-1-positive cells and MIB-5-positive cells were decreased by HRI in hearts and kidneys almost to levels observed in normotensive Sprague-Dawley rats. The renoprotective effects of HRI were at least in part due to improved renal hemodynamics and distal tubular function, since HRI shifted renal pressure-diuresis/natriuresis curves leftward by approximately 35 mm Hg, increased glomerular filtration rate and renal blood flow, and shifted the fractional water and sodium excretion curves leftward. In untreated dTGR, plasma Ang II was increased by 400% and renal Ang II level was increased by 300% compared with Sprague-Dawley rats. HRI decreased plasma human renin activity by 95% and normalized Ang II levels in both plasma and kidney compared with triple-drug therapy. Our findings indicate that in dTGR harboring human renin and angiotensinogen genes, Ang II causes end-organ damage and promotes inflammatory response and cellular growth largely independent of blood pressure.

Albuminuria↗

Effect of bosentan on NF-kappaB, inflammation, and tissue factor in angiotensin II-induced end-organ damage.

Reports on the effectiveness of endothelin receptor blockers in angiotensin (Ang) II-induced end-organ damage are conflicting, and the mechanisms involved are uncertain. We tested the hypothesis that endothelin (ET)(A/B) receptor blockade with bosentan (100 mg/kg by gavage after age 4 weeks) ameliorates cardiac and renal damage by decreasing inflammation in rats harboring both human renin and angiotensinogen genes (dTGR). Furthermore, we elucidated the effect of bosentan on tissue factor (TF), which is a key regulator of the extrinsic coagulation cascade. We compared bosentan with hydralazine (80 mg/L in the drinking water for 3 weeks) as a blood pressure control. Untreated dTGR featured hypertension, focal necrosis in heart and kidney, and a 45% mortality rate (9 of 20) at age 7 weeks. Compared with Sprague-Dawley controls, both systolic blood pressure and 24-hour albuminuria were increased in untreated dTGR (203+/-8 versus 111+/-2 mm Hg and 67.1+/-8.6 versus 0.3+/-0.06 mg/d at week 7, respectively). Bosentan and hydralazine both reduced blood pressure and cardiac hypertrophy. Mortality rate was markedly reduced by bosentan (1/15) and partially by hydralazine (4/15). However, only bosentan decreased albuminuria and renal injury. Untreated and hydralazine-treated dTGR showed increased nuclear factor (NF)-kappaB and AP-1 expression in the kidney and heart; the p65 NF-kappaB subunit was increased in the endothelium, vascular smooth muscles cells, infiltrating cells, glomeruli, and tubules. In the heart and kidney, ET(A/B) receptor blockade inhibited NF-kappaB and AP-1 activation compared with hydralazine treatment. Macrophage infiltration, ICAM-1 expression, and the integrin expression on infiltrating cells were markedly reduced. Renal vasculopathy was accompanied by increased tissue factor expression on macrophages and vessels of untreated and hydralazine-treated dTGR, which was markedly reduced by bosentan. Thus, ET(A/B) receptor blockade inhibits NF-kappaB and AP-1 activation and the NF-kappaB- and/or AP-1-regulated genes ICAM-1, VCAM-1, and TF, independent of blood pressure-related effects. We conclude that Ang II-induced NF-kappaB and AP-1 activation and subsequent inflammation and coagulation involve at least in part the ET(A/B) receptors.

Albuminuria↗

Is there a psoriatic osteopathy? -- the activity of bone resorption in psoriatics is related to inflammatory joint process.

The aim of this study was to examine former own histomorphological results by using biochemical markers of bone collagen catabolism in patients with psoriasis vulgaris and psoriatic arthritis and to compare these results with those from rheumatoid arthritis. - The diagnosis of PsA was made according to the diagnostic criteria of Moll and Wright modified by Bennet. Urine was collected from 99 patients with PsA, 21 patients suffering from PS without articular manifestations, 154 patients with RA fulfilling the ACR criteria of 1987, and 80 healthy controls. Pyridinoline and deoxypyridinoline in urine were analyzed by HPLC, levels of CrP and ESR were estimated using laboratory assessment. - Both crosslinks show a elevated excretion in PsA (particularly in active PsA / aPsA) as well as in RA. PS and Controls show no significant difference in the elimination of crosslinks. The levels of both crosslinks are higher in females than males in all groups. With the exception of Dpyd levels in urine which only show a tendency to correlate with ESR, there are positive correlations between measured crosslink-levels in urine and markers of inflammation. The Pyd/Dpyd ratio displays a significant correlation with ESR. - An increased breakdown of collagen I and II was found only in active forms of psoriatic arthritis and in rheumatoid arthritis. Our biochemical results do not demonstrate a complete agreement with former scintigraphic or histological investigations of other authors and own histomorphological results.

Adult↗

[Creatinine and calcium in urine and blood after brief exposure to magnetic fields].

In this experimental study, 35 males were exposed to artificial magnetic fields. The fields were produced by a set of Helmholz coils internally isolated by a Faraday cage which effectively eliminated electrical fields. Each participant stayed inside the coils for 40 minutes on two occasions with an interval of seven days, but was actually only once exposed to a static magnetic field (9.6 mT) and oscillating magnetic fields of variable frequency and strength. Urine and blood samples were taken before and after exposure, and before and after non-exposure. Analysis detected significant changes in serum creatinine level after exposure (p < 0.0001). The changes in serum creatinine level in the nonexposed situation were significantly smaller than the changes found in the exposed situation (p < 0.0001). The changes i urine creatinine after 40 minutes of exposure was also found to be significant (p < 0.01). Exposure to magnetic fields may induce biological reactions.

Adult↗

[MR imaging-guided interventions].

The spectrum of MR imaging-guided interventions includes biopsies, thermal ablation modalities, vascular applications, MR endoscopy and intraoperative MR imaging. The concept of MR guidance is based on the excellent morphologic and functional imaging achieved by MR. The most important recently published experimental and clinical results are discussed. In the future, MR imaging will play an important role in interventional radiology, minimal invasive therapy and guidance of surgical procedures.

Biopsy↗

The impact of ergotamine-induced headache and ergotamine withdrawal on information processing.

Ergotamine abuse and subsequent ergotamine-induced headache is a common problem in the pharmacological treatment of migraine and other headache types; often, withdrawal therapy is necessary. This study investigated whether ergotamine abuse affects information processing and whether withdrawal therapy can lead to an improvement of information processing. We designed a standardized neurophysiological retrospective (ergotamine abuse) and prospective (ergotamine withdrawal) study in a supraregional headache outpatient clinic. Seventy-one patients abusing ergotamine derivatives with subsequent daily headache were enrolled and compared to 36 migraine patients without ergotamine intake and 36 healthy subjects. Information processing was evaluated by latencies and amplitudes of visually evoked event-related potentials (ERP) before and after ergotamine withdrawal therapy. P3 latency of the ERP was significantly increased in ergotamine abuse (442 +/- 45 ms) versus migraine (415 +/- 40 ms) and healthy subjects (410 +/- 33 ms), there was no difference between ergotamine tartrate and dihydroergotamine abuse. The migraine specific loss of habituation in information processing as measured by P3 latency could not be observed in migraine patients with ergotamine abuse. After successful withdrawal therapy in 36 patients, the abnormally prolonged P3 latency was significantly shortened (452 +/- 47 ms versus 433 +/- 30 ms; P < 0.004). Our findings imply that information processing is impaired by ergotamine abuse and can be improved but not normalized after withdrawal therapy. Furthermore, our data provide strong evidence that ergotamine, besides its peripheral effects, has a central mode of action.

Adrenergic alpha-Agonists↗

Preliminary experience with interactive guided brain biopsies using a vertically opened 0.5-T MR system.

The purpose of our study was to evaluate the feasibility and accuracy of brain biopsies performed within a vertically opened MR system. We worked with the interventional 0.5-T MR "SIGNA SP" (General Electric Medical Systems, Milwaukee, Wis.) with an integrated tracking device "Flashpoint Position Encoder" (Image Guided Technologies, USA). As a holding device for this instrument we constructed a special frame. The whole system allows an exact adjustment of an optimum biopsy direction and guidance of the biopsy in a non-stereotactic, interactive mode in near real-time. As biopsy tools we used MR-compatible aspiration and specially made side-cut needles (Daum, Germany; E-Z-EM, USA). We performed a prospective diagnostic brain biopsy study in 18 patients. Guidance of the needle was carried out using gradient-echo single-slice technique. The sample was taken after controlling the exact position of the needle tip on spin-echo images. In 12 cases an exact neuropathological diagnosis was possible. In 6 cases of negative biopsy (4 aspiration biopsies) the samples were not representative. Our results demonstrate the feasibility of interactive MR-guided minimally invasive brain biopsies in an open MR system. The best results were achieved using cut needles for biopsies of contrast-enhancing lesions visible on T1-weighted gradient-echo guidance sequence.

Adult↗

Chondromatosis of the ankle joint (Reichel syndrome).

A case of chondromatosis of the upper ankle joint in childhood is described. It is a monoarticular disease with a good prognosis, frequently without known prior trauma or inflammation, although often free fragments of cartilage are seen in the joint cavities. It originates from the synovium of the joint, and is known in the literature as Reichel syndrome.

Acute Disease↗

Open MR imaging in spine surgery: experimental investigations and first clinical experiences.

INTRODUCTION: The latest open MRI technology allows to perform open and closed surgical procedures under real-time imaging. Before performing spinal trauma surgery preclinical examinations had to be done to evaluate the artifacts caused by the implants. METHODS: The MRT presented is a prototype developed by GE. Two vertically positioned magnetic coils are installed in an operation theater. By that means two surgeons are able to access the patient between the two coils. Numerous tests regarding the material of instruments and implants were necessary in advance. The specific size of the artifact depending on the pulse sequence and the positioning within the magnetic field had to be examined. RESULTS: The magnifying factors of the artifact in the spin echo sequence regarding titanium are between 1.7 and 3.2, depending on the direction of the magnetic vector. Regarding stainless steel they are between 8.4 and 8.5. In the gradient echo sequence the factors are between 7.5 and 7.7 for titanium and between 16.9 and 18.0 for stainless steel. The tip of an implant is imaged with an accuracy of 0 to 2 mm. Since September 1997 16 patients with unstable fractures of the thoracic and lumbar spine have been treated by dorsal instrumentation in the open MRI. Percutaneous insertion of the internal fixator has proven a successful minimally invasive procedure. The positioning of the screws in the pedicle is secure, the degree of indirect reduction of the posterior wall of the vertebral body can be imaged immediately. The diameter of the spinal canal can be determined in any plane. DISCUSSION AND CONCLUSION: The open MRI has proven useful in orthopedic and trauma surgery. The size and configuration of the artifacts caused by instruments and implants is predictable. Therefore exact positioning of the implants is achieved more easily. Dorsal instrumentation of unstable thoracolumbar fractures with a percutaneous technique has turned out safe and less traumatic under MR-imaging. Real-time imaging of soft tissue and bone in any plane improves security for the patient and allows the surgeon to work less invasively and more precisely.

Artifacts↗

Open MRI-guided neurosurgery.

OBJECTIVES: A number of different image-guided surgical techniques have been developed during the past decade. None of these methods can provide the surgeon with information about the dynamic changes that occur intra-operatively. MATERIAL AND METHOD: The first vertical open 0.5T MRI-scanner for intra-operative MRI-guided neurosurgery in Germany was installed at the University of Leipzig during the summer 1996. Since autumn 1996 a number of surgical procedures including biopsies (n = 31), craniotomies (n = 32), transsphenoidal procedures (n = 8) and interstitial lasertherapies (n = 3) have been performed using intra-operative MR image guidance. RESULTS: The development of MR-compatible and MR-safe non-magnetic instruments and components had to be solved. Specific surgical instruments were developed to perform biopsies, craniotomies, microsurgical tumour resections and transsphenoidal procedures in the 0.5-T open MRI. Several components required adaptation including the head holder the stereotactic navigation device, the high speed drill, the suction unit, the ultrasonic aspirator, the bipolar coagulation, the laser probe and the surgical microscope. All these newly developed technical features enable the neurosurgeon to perform a large number of surgical procedures under direct control and guidance of intra-operative MR imaging. In contrast to frame-based for framless navigation systems, intra-operative MRI provides accurate and immediate information during the progress of surgery. These intra-operative images allow definitive localization and targeting of the lesions and accommodate anatomical changes that may occur during surgery. CONCLUSION: Intra-operative MRI is helpful for navigation as well as determining of tumour margins to achieve a complete and safe resection of intracranial lesions. Complications related to the surgical procedure are reduced and the risk of neurological deterioration due to tumour removal and postoperative complications is minimized. It can be concluded that the intra-operative application of interventional MRI technology may represent a major step forward in the field of neurosurgery.

Biopsy↗