[Is a decompressive hemicraniectomy sensible in space occupation through stroke or head and brain trauma?].
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Biomedical subjects
Publications and source records attributed to B Neundörfer.
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Signal shortening of the motor cortex in T2-weighted MR images is a frequent finding in patients with amyotrophic lateral sclerosis (ALS). The cause of signal shortening in ALS is unknown, although iron deposits have been suggested. To test this hypothesis, we acquired T2*-weighted gradient-echo (GRE) MR images in addition to T2-weighted turbo spin-echo in 69 patients with ALS. Signal shortening in T2-weighted images was found in 31 patients. In T2*-weighted GRE images, only three patients had signal shortening. One patient with additional bifrontal haemorrhage had frontal but no motor cortex signal shortening. Iron deposits do not cause cortical signal shortening in patients with ALS predominantly. Other factors are presumably more important in the generation of cortical T2 shortening in ALS.
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Oxidative stress and nuclear factor-kappaB (NF-kappaB) activation are linked to the pathogenesis of many metabolic, degenerative, and chronic inflammatory diseases. Activation of the receptor for advanced glycation end products (RAGE) by its specific ligand N(epsilon)-carboxymethyllysine (CML) results in the activation of NF-kappaB and the production of proinflammatory cytokines. To determine whether engagement of RAGE contributes to the pathogenesis of inflammatory myopathies, we performed immunohistochemical studies on the presence of CML-modified proteins, RAGE and activated NF-kappaB in muscle biopsies of patients with polymyositis (PM, n=10), dermatomyositis (DM, n=10), limb girdle muscular dystrophy (LGMD, n=10) and in 10 controls with normal muscle biopsy results. In inflammatory myopathies CML, RAGE and NF-kappaB were detected in mononuclear cells and in regenerating muscle fibers. CML, NF-kappaB and, to a lesser extent, RAGE were also found in degenerating muscle fibers, but colocalization of CML, RAGE and NF-kappaB was only seen in infiltrating mononuclear cells and regenerating muscle fibers. Immunofluorescence double labeling demonstrated an expression of CML, RAGE and NF-kappaB in CD4-, CD8-, CD22- and CD68-positive mononuclear cells. Western blot analysis showed an increased immunoreactivity for CML-modified proteins in PM and DM. In LGMD, CML, RAGE and NF-kappaB were found in regenerating muscle fibers and less frequently in degenerating muscle fibers, and with lower staining intensities than in inflammatory myopathies. Our data suggests that the CML-RAGE-NF-kappaB pathway is an evident proinflammatory pathomechanism in mononuclear effector cells in PM and DM. RAGE-mediated NF-kappaB activation may be involved in muscle fiber regeneration in inflammatory myopathies and LGMD.
The purpose of our study was to evaluate inter- and intra-subject variability and scan-rescan reproducibility of single-voxel 1H-MR spectroscopy (1H-MRS) in hippocampal structures at 1.5 T field strength. Thirty healthy adults were studied bilaterally by optimized, standardized short echo time single-voxel 1H-MRS (PRESS, TE=30 ms, TR=3000 ms, oblique voxel orientation, voxel size 2 cm3). Spectral analysis and absolute metabolite quantitation of N-acetylaspartate+N-acetylaspartyl-glutamate (tNAA), choline (Cho), creatine (Cr), total glutamate plus glutamine (Glu+Gln) and myo-inositol (Ins) were carried out by LCModel. Inter- and intra-individual reproducibility of these metabolite values were investigated by calculation of mean, standard deviation, coefficient of variation (CV), and by analysis of variance for repeated measurements. The smallest CV in intersubject variability was obtained for tNAA, followed by Cr, Cho, Ins and Glu+Gln. The results of the analysis of variance for repeated measures in inter-subject variability showed a marginal effect of scan repetition for Cr (p=0.063) and Glu+Gln (p=0.082); the rescan of both metabolites showed slightly higher concentrations. No statistical significant effect of scan repetition was seen for tNAA (p=0.913), Cho (p=0.857), and Ins (p=0.826). Rescan led to the same results and gave proof of good reproducibility. Scan-rescan testing in one subject showed comparable results: tNAA (CV=4.8%), followed by Cr, Ins, Glu+Gln and Cho (all CV above 10%).
Modern stroke care requires urgent initiation of treatment. Thus, rapid recognition of cerebrovascular incidents by medical laypersons is mandatory. Accordingly, public knowledge of stroke warning signs and adequate action is very important. Little is known about the level of knowledge among the general public and use and effect of various sources of information. In first aid training programs conducted by the St. John Ambulance in Bavaria, participants were questioned if and from what source they already got information about stroke. Additionally they were asked to list stroke warning signs and to describe what a stroke is. Altogether 532 subjects filled out the questionnaire; 419 stated that they already had heard something about stroke (53.7% male, mean age 29.4 years). Sources of information were: personal experience with affected patients (30.1%), TV/radio (22.1%), newspaper (18.4%) and relatives/friends (17.2%). Subjects with prior information listed significantly more warning signs/symptoms compared with those without previous information (1.76 vs. 0.63; p<0.01). Participants using the source "TV/radio" named fewer warning signs than those using the sources "newspaper" or "affected patients" (p<0.01). Prior information was effective in enhancing knowledge about stroke. However, we found significant differences related to the source of information. Since experiences gathered from personal contact with affected patients were stated most frequently, leading to better knowledge than information gained from mass media, subsequently acute care and rehabilitation would be a good opportunity for providing information about stroke to proxies and visitors of the patients.
Low back pain is often treated with paraspinal injections of analgesics and steroids. Infectious complications of these techniques are rare but they can potentially hold high risks for the patients. History and clinical data of all patients admitted to a neurological unit suffering from community acquired purulent meningitis were prospectively analyzed during an 8 year interval (1992 and 2000) with special regard to the previous medical history. One hundred and twenty eight patients were included in the study. Eight out of 128 patients (6.25%) had a history of single or repeated paravertebral (4/8), facet-joint (2/8), peridural (1/8) or spinal (1/8) injections 2-21 days before admission to the hospital. In six out of eight patients either Staphylococcus aureus (4/8) or coagulase-negative staphylococci (2/8) were found in the cerebro spinal fluid (CSF), in two patients no causative organism was detected. One patient died, three survived with sequel. Repeated paraspinal, peridural or spinal injections with analgesic drugs in combination with corticosteroids hold a risk for parameningeal inoculation of bacteria resulting in paraspinal, spinal, and epidural abscesses or meningitis. The absolute frequency of these complications may be rare but they are responsible for a considerable proportion of community acquired purulent CNS infections.
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Binding of ligands to the receptor for advanced glycation end products (RAGE) results in activation of the transcription factor nuclear factor kappa B (NF-(kappa)B) and subsequent expression of NF-(kappa)B-regulated cytokines. This has been shown to be a relevant pathomechanism in diabetic polyneuropathies (PNP). To determine whether this pathway may contribute to the pathogenesis of PNP due to impaired glucose tolerance (IGT) we performed a pilot study to demonstrate the presence of the RAGE ligand N (epsilon)-(Carboxymethyl)lysine (CML), the receptor itself and N-(kappa)B in sural nerve biopsies of 4 patients with IGT-related PNP. Biopsies of either 4 patients with diabetic PNP and with Charcot-Marie-Tooth disease (CMT) I and II served as positive and negative controls, respectively. In IGT-related PNP and diabetic PNP, CML, RAGE, and NF-(kappa)B was found in the perineurium, epineurial vessels and in part in endoneurial vessels. CMT patients showed, if any, only weak staining for one or the other antigen. These data suggest that activation of the RAGE pathway may be one of the first steps in the pathogenesis of PNP even before chronic hyperglycemia occurs.
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OBJECTIVES: The aim of this study was to assess baroreflex regulation of the heart rate and blood vessels in migraine patients in comparison with healthy controls. METHODS: In 30 migraine patients who were in a headache-free phase, aged 34 +/- 2 years, and 30 healthy controls, aged 34 +/- 3 years, we applied oscillatory neck suction at 0.1 Hz to assess the sympathetic modulation of the heart and blood vessels and at 0.2 Hz to assess the effect of parasympathetic stimulation on the heart. Breathing was paced at 0.25 Hz. Electrocardiographic RR-intervals, blood pressure and respiration were continuously recorded. Responses to the baroreflex stimulations were assessed as the changes in power of the RR-interval and blood pressure fluctuations at the relevant stimulating frequency from the baseline values. RESULTS: Systolic and diastolic blood pressure responses to the 0.1 Hz neck suction pressure were not significantly different between the patients and controls. The RR-interval oscillatory response to 0.2 Hz neck suction was significantly less (P < 0.05) in the migraine patients (4.45 +/- 0.27 ln ms2) compared with the controls (5.48 +/- 0.36 ln ms2). CONCLUSION: These results suggest that baroreflex-mediated cardiovagal responses are reduced in migraine patients. However, the sympathetic-mediated baroreflex control of the blood vessels is intact in the migraine patients. The autonomic nervous system may have a role in the pathophysiology of migraine.
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BACKGROUND: Patients with atypical neuralgia or atypical facial pain have been surgically treated with microvascular decompression (MVD) of the trigeminal root entry zone (TREZ). There are no data regarding the sensitivity and specificity of a vessel-TREZ relationship as a cause of pain in patients with persistent idiopathic facial pain (PIFP) according to the definition given by the International Headache Society (IHS). METHODS: The TREZ was visualised by 3D CISS MRI in 12 patients with unilateral PIFP according to the IHS criteria. RESULTS: The frequency of artery-TREZ, vein-TREZ, or vessel (artery/vein)-TREZ contacts on the symptomatic and asymptomatic sides did not differ significantly. On the symptomatic side, vessel-TREZ contact was found in 58% of patients (sensitivity). On the asymptomatic side, vessel-TREZ contact was absent in 33% of patients (specificity). CONCLUSIONS: On the basis of the low sensitivity and specificity found in the present study, PIFP cannot be attributed to a vessel-TREZ contact, and therefore, pain relief after MVD cannot be expected.
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UNLABELLED: Increasing evidence has suggested that oxidative stress may be involved in the pathogenesis of amyotrophic lateral sclerosis (ALS). The antioxidant vitamin E (alpha-tocopherol) has been shown to slow down the onset and progression of the paralysis in transgenic mice expressing a mutation in the superoxide dismutase gene found in certain forms of familial ALS. The current study, a double blind, placebo-controlled, randomised, stratified, parallel-group clinical trial, was designed to determine whether vitamin E (5000 mg per day) may be efficacious in slowing down disease progression when added to riluzole. METHODS: 160 patients in 6 German centres with either probable or definite ALS (according to the El Escorial Criteria) and a disease duration of less than 5 years, treated with riluzole, were included in this study and were randomly assigned to receive either alpha-tocopherol (5000 mg per day) or placebo for 18 months. The Primary outcome measure was survival, calculating time to death, tracheostomy or permanent assisted ventilation, according to the WFN-Criteria of clinical trials. Secondary outcome measures were the rate of deterioration of function assessed by the modified Norris limb and bulbar scales, manual muscle testing (BMRC), spasticity scale, ventilatory function and the Sickness Impact Profile (SIP ALS/19). Patients were assessed at entry and every 4 months thereafter during the study period until month 16 and at a final visit at month 18. Vitamin E samples were taken for compliance check and Quality Control of the trial. For Safety, a physical examination was performed at baseline and then every visit until the treatment discontinuation at month 18. Height and weight were recorded at baseline and weight alone at the follow-up visits. A neurological examination as well as vital signs (heart rate and blood pressure), an ECG and VEP's were recorded at each visit. Furthermore, spontaneously reported adverse experiences and serious adverse events were documented and standard laboratory tests including liver function tests performed. For Statistical Analysis, the population to be considered for the primary outcome measure was an "intent-to-treat" (ITT) population which included all randomised patients who had received at least one treatment dose (n = 160 patients). For the secondary outcome measures, a two way analysis of variance was performed on a patient population that included all randomised patients who had at least one assessment after inclusion. RESULTS: Concerning the primary endpoint, no significant difference between placebo and treatment group could be detected either with the stratified Logrank or the Wilcoxon test. The functional assessments showed a marginal trend in favour of vitamin E, without reaching significance. CONCLUSION: Neither the primary nor the secondary outcome measures could determine whether a megadose of vitamin E is efficacious in slowing disease progression in ALS as an add-on therapy to riluzol. Larger or longer studies might be needed. However, administration of this megadose does not seem to have any significant side effects in this patient population.
The authors investigated 17 patients with idiopathic intracranial hypertension (IIH), correlating laser scanning tomography of the optic nerve with CSF opening pressure. The decrease in papilla volume and papilla height showed a linear correlation with the opening pressure of the CSF (r = 0.59, p < 0.001; r = 0.63, p < 0.001). If the CSF opening pressure is higher than 20 cm water, an increase of 5 cm water CSF pressure corresponds to a papilla volume increase of 0.95 mm3 as well as a papilla height increase of 0.34 mm.