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Pyogenic infections of the central nervous system of dental origin are quite uncommon in industrialized countries. We report six cases with intracerebral (n = 4) and intraspinal (n = 2) infections treated in our hospital. The microbial pathogen was successfully isolated in all patients. Fusobacterium nucleatum as well as Streptococcus species were found in three cases. Bacillus species were identified in two patients. Actinomyces was the etiologic agent in one case. All patients suffered from dental pathologies, so that after clinical and radiological exclusion of other sources an oral focus was presumed. Therapeutic management consisted of an operative procedure in order to obtain decompression, as well as evacuation of the pus on the one hand, followed by targeted antibiotics on the other. Clinical improvement was achieved in all patients, with one patient lost to follow-up. On magnetic resonance tomography, the inflammatory changes also disappeared in all cases. We recommend that oral infection with recurrent bacteraemia should always be considered in the pathogenesis of the so-called "cryptic" intracerebral and intraspinal infections.

In patients undergoing lung surgery, single intercostal nerve block plus i.v. patient-controlled analgesia with morphine is not as effective as patient-controlled EDA with respect to pain control and restoration of pulmonary function.

-resolution single-nucleotide polymorphism array-profiling in myeloproliferative neoplasms identifies novel genomic aberrations. Haematologica. 2010;95: 666-669. doi:10.3324/haematol.2009 This is an open-access paper. ABSTRACT © F e r r a t a S t o r t i F o u n d a t i o ngain of 1q (n=4), and trisomy 8 (n=4), followed by loss of 5q11-q13 and 13q12-q21 in single cases (Table 1). While 20q losses occurred in all MPN subgroups, gain of 9p / trisomy 9 was restricted to PV and secondary MF patients, and trisomy 8 to PMF patients. Gain of 1q was observed in one PV, one ET, and 2 PMF cases. In addition, SNP-profiling revealed two recurrent small CNAs that were undetectable in cytogenetic studies: 11 ET and 2 PV patients showed small gains in 10q11.22 (1.5-2.7 Mb), whereas one post-ET and one post-PV MF case exhibited microdeletions in 17q11.2 (1.6 and 2.7 Mb, respectively) encompassing the tumor suppressor gene Neurofibromatosis-1 (NF1).To validate these findings, matched pair analysis using germline and tumor material was performed in a subset of these cases. Skin biopsies were taken from 2 patients with 10q11 gain and from one patient with 17q11 loss. SNPprofiles revealed that 10q11 gains represented CNVs in both cases, whereas the tumor-specific origin of cryptic deletion in 17q11 was confirmed (Figure 1). The disclosure of the 10q11 CNV reduced the frequency of detected CNAs in ET and PV to 11% each. Furthermore, fluorescence in situ hybridization performed in both cases with loss in 17q11 showed monoallelic NF1 deletion in nearly 100% of the metaphase and interphase cells. Mutation analysis revealed a single base pair deletion in exon 5 (c.528delT) leading to a stop codon in the post-PV MF patient, whereas in the post-ET case no sequence variations were detected. With regard to the clinical phenotype in both patients MF was secondary to a prior ET or PV, respectively. Both cases were characterized by a progressive clinical course and both patients underwent allogeneic stem cell transplantation. Of note, the patient with monoallelic NF1 deletion reached a sustained complete remission, whereas the patient with biallelic NF1 alteration transformed into acute myeloid leukemia three months after transplantation and died.NF1 is associated with the hereditary von Recklinghausen's neurofibromatosis. It has been shown that these patients have an increased risk of developing various tumors including myeloid leukemias.5 NF1 functions as a negative regulator of the RAS signal transduction pathway, and loss of NF1 can lead to a progressive myeloproliferative disorder.6 Cases with cryptic deletions in 17q11 encompassing NF1 have been identified in several recent studies on adult and childhood acute myeloid and T-lymphoblastic leukemia patients as well as in PMF patients. [7][8][9][10] In addition, Balgobind et al. identified in 3 out of 4 childhood leukemia patients with monallelic NF1 deletions truncating mutations in the remaining allele, that resulted in biallelic inactivation of the gene.9 Taken together, these data stro...

The surgical management of cervical spondylodiscitis consists of the resection of the affected disc, the decompression of the cervical spinal cord, followed by the stabilization using an autologous bone graft or a titanium implant combined with a ventral plate fixation. Until now, there were no studies about the practicability and putative safety of PEEK cages in cervical spine infection. Now, we present the history of five patients suffering from neurological deficits and septicemia caused by mono- or bisegmental pyogenic cervical discitis and intraspinal abscess without severe bone destruction. Patients were treated surgically by discectomy, decompression, and ventral spondylodesis. The disc was replaced by a PEEK cage without additional fixation. Progressive bony fusion and complete regression of the inflammatory changes was demonstrated 7-8 months later by a computer assisted tomography and contrast enhanced magnetic resonance imaging, respectively. The vertebral alignment changed minimally; the cages developed only a slight average subsidence. The clinical symptoms improved in all patients significantly. Neck pain or instability was never observed. Nevertheless, prospective investigations of a larger patient series are mandatory. We suppose that the use of PEEK cages represents a potential and safe alternative in the treatment of cervical spondylodiscitis in selected patients.

The operative treatment of subcortical metastatic tumours within the paracentral area is still under discussion. Against the background of possible new postoperative neurological deficits and of evolving new radio oncological techniques, the indication for surgery is limited only to a subgroup of patients. In this retrospective study we present the clinical results after operative treatment of metastases within the central and paracentral brain region, with an emphasis on the short-term and mid-term functional outcome. We report on 20 patients suffering from subcortical brain metastases within the primary sensorimotor area, with a median volume on MRI-scans of 8.18 cm³. Patients were admitted to our department with a progressive hemiparesis (n = 11), focal seizures (n = 6) or other unspecific symptoms (n = 3) like headache, nausea, and neuropsychological disturbances, respectively. After updated MRI- and fMRI-scanning, intensive electrophysiological testing including MEP-brain mapping and interdisciplinary tumour-board discussion of each case, those patients were evaluated for surgery. Early postoperative control was done by MRI within the first 48 h. Follow-up took place in our outpatient department, assessing clinical criteria two and 6 weeks postoperatively, followed by clinical control and MRI-scans every 3 months. In all patients, surgery was performed under general anaesthesia, cranial neuro navigation and intraoperative motor cortex stimulation. Surgery and the early postoperative course were uneventful in all cases. After a 6 months follow-up, two patients had died. The motor deficits improved in seven patients and remained unchanged in four cases. One patient suffered from a new persistent hemiparesis. A temporary paresis occurred in two cases. In five patients there was no motor deficit pre- and postoperatively. The Karnofsky Performance Status improved in ten patients 6 months after surgery. Quality of Life, measured by the FACT-Br score, improved in 12 patients and remained unchanged in one patient. With modern techniques like fMRI-guided cranial neuronavigation and intraoperative neuromonitoring including direct stimulation of the motor cortex, microsurgical resection of subcortical paracentral metastases is feasible with an acceptable risk of neurological deterioration. Even preexistent deficits can improve with positive influence on the quality of life for oncological patients, being disabled by the symptoms caused by the cerebral lesion.

The expression of functional GABA(A)-receptors in glioma cells correlates with low malignancy of tumours and cell lines from glioma lack these receptors. Here we show that contact with neurons induces the expression of functional GABA(A)-receptors. C6 and F98 glioma cell lines were labelled by recombinant expression of enhanced green fluorescent protein injected into rat brain and studied in acute slices after two to three weeks of tumour growth. The cells responded to GABA or the specific agonist, muscimol with a current typical for GABA(A)-receptors, as studied with the patch-clamp technique. To get insight into the mechanism of GABA(A) receptor induction, the C6 or F98 cells were co-cultured with neurons, astrocytes, oligodendrocytes and microglia. Glioma cells expressed functional GABA(A) receptors within 24 h only in cultures where physical contact to neurons occurred. Activation of GABA(A)-receptors in the co-cultures attenuated glioma cell metabolism while blockade of the receptors increased metabolism. We conclude that with this form of interaction, neurons can influence tumour behaviour in the brain.