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Studies on preemptive analgesia in maxillofacial surgery have shown several controversial clinical results, mainly due to the absence of a methodological standard, besides a wide variety of studied drugs. This study intended to answer the following hypothesis: Is the administration of dipyrone preemptively capable of decreasing trans- and postoperative pain in the third molar surgical extraction?
A pilot prospective double-blind placebo-controlled study was carried out with 25 patients submitted to the third molar surgical extraction at two moments, one side in each intervention. Dipyrone (1 g) was preemptively administered (study group) for the extraction of two third molars on the same side and, in a second surgical procedure, dipyrone (1 g) was administered in the immediate postoperative period (control group). Evaluated variables were the amount of anesthetic, pain perceived through the visual analogue scale (VAS) in transoperative and immediate postoperative periods, and over 12-h investigation period, analgesic consumption, duration of surgery, and time to rescue analgesia.
The results were submitted to Student's t test and statistical differences were observed in transoperative (p < 0.05) and immediate postoperative (p < 0.01) periods, while the other studied variables did not present statistical differences.
The preemptive administration of dipyrone decreased the perception of transoperative and immediate postoperative pain when compared to its use after surgery only.
Studies on preemptive analgesia in maxillofacial surgery have shown several controversial clinical results, mainly due to the absence of a methodological standard, besides a wide variety of studied drugs. This study intended to answer the following hypothesis: Is the administration of dipyrone preemptively capable of decreasing trans- and postoperative pain in the third molar surgical extraction?
A pilot prospective double-blind placebo-controlled study was carried out with 25 patients submitted to the third molar surgical extraction at two moments, one side in each intervention. Dipyrone (1 g) was preemptively administered (study group) for the extraction of two third molars on the same side and, in a second surgical procedure, dipyrone (1 g) was administered in the immediate postoperative period (control group). Evaluated variables were the amount of anesthetic, pain perceived through the visual analogue scale (VAS) in transoperative and immediate postoperative periods, and over 12-h investigation period, analgesic consumption, duration of surgery, and time to rescue analgesia.
The results were submitted to Student's t test and statistical differences were observed in transoperative (p < 0.05) and immediate postoperative (p < 0.01) periods, while the other studied variables did not present statistical differences.
The preemptive administration of dipyrone decreased the perception of transoperative and immediate postoperative pain when compared to its use after surgery only.
Recent investigations are focused on the potential antitumor effect of neurokinin-1 receptor (NK1R) antagonists in different neoplastic diseases1. Consequently, Kwatra et al. raised an interesting observation about the possible influence of aprepitant on CTCL outcome2.
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Itch pathogenesis involves modulation of the neuroimmune axis, with several immunosuppressants such as azathioprine1 and mycophenolate mofetil2 demonstrating significant anti-pruritic activity in subsets of patients with pruritus. These immunosuppressive agents are contraindicated in patients with malignancy, and thus there is a need for novel anti-pruritic agents without significant immunosuppressive effects in neoplastic conditions such as cutaneous T cell lymphoma (CTCL).
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The recent technology of 3D cultures of cellular aggregates derived from human stem cells have led to the emergence of tissue-like structures of various organs including the brain. Brain organoids bear molecular and structural resemblance with developing human brains, and have been demonstrated to recapitulate several physiological and pathological functions of the brain. Here we provide an overview of the development of brain organoids for the clinical community, focusing on the current status of the field with an critical evaluation of its translational value.
Journal of Neurotrauma , Vol. 0, No. 0.
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Athletes experience various situations and conditions that can interfere with their sleep, which is crucial for optimal psychological and physiological recovery as well as subsequent performance. Conventional sleep screening and intervention approaches may not be efficacious for athletes given their lifestyle, the demands of training and travel associated with interstate/international competition.
The present systematic review aimed to summarize and evaluate sleep intervention studies targeting subsequent performance and recovery in competitive athletes. Based on the findings, a secondary aim was to outline a possible sleep intervention for athletes, including recommendations for content, mode of delivery and evaluation.
A systematic review was conducted based on the PRISMA guidelines in May 2016 with an update completed in September 2017. Ten studies met our inclusion criteria comprising a total of 218 participants in the age range of 18–24 years with athletes from various sports (e.g., swimming, soccer, basketball, tennis). A modified version of the quality assessment scale developed by Abernethy and Bleakley was used to evaluate the quality of the studies.
The included studies implemented several sleep interventions, including sleep extension and napping, sleep hygiene, and post-exercise recovery strategies. Evidence suggests that sleep extension had the most beneficial effects on subsequent performance. Consistent with previous research, these results suggest that sleep plays an important role in some, but not all, aspects of athletes' performance and recovery.
Future researchers should aim to conduct sleep interventions among different athlete populations, compare results, and further establish guidelines and intervention tools for athletes to address their specific sleep demands and disturbances.
Future Oncology, Ahead of Print.
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Future Oncology, Ahead of Print.
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Journal of Neurotrauma , Vol. 0, No. 0.
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Children with inflammatory bowel disease (IBD) or autoimmune hepatitis (AIH) are at risk for severe infections. This is partially a result of their chronic disease condition but, moreover, a side effect of their immunosuppressive therapy. Currently, vaccinations with live vaccines are regarded as contraindicated under immunosuppressive therapy, mainly because of concerns about side effects and a lack of data showing an adequate immune reaction. As there is no systematic study on the individual immunoreactivity under immunosuppressive therapy in this patient group, we analyzed the lymphocyte subgroups and immunoreactivity of lymphocytes in children with IBD or AIH with and without immunosuppressive therapy in vitro.
We collected whole blood samples from 17 children with IBD or AIH on high-level immunosuppression (IS) (group 1) and 8 on low-level IS (group 2) in comparison with 6 patients without systemic IS (group 3). After Ficoll separation of peripheral mononuclear cells, the samples were analyzed by flow cytometry to determine the lymphocyte subgroups. Furthermore, we stimulated the isolated lymphocytes with phytohemagglutinin (PHA), tetanus antigen, and adenovirus antigen and measured their proliferation by incorporation of H3-thymidine detected in a beta counter.
The statistical evaluation was performed by Kruskal-Wallis test and Mann-Whitney U test using a bilateral level of significance of α = 5%.
Patients with low- or high-level IS showed no significant difference in the number of lymphocytes or T cells.
Interestingly, IS did not influence the lymphocyte proliferation assay significantly regarding median reaction to PHA, tetanus antigen, or adenovirus antigen between the three groups. However, comparing all immunosuppressed patients to the patients without IS, there was a significant difference towards stimulation with tetanus antigen.
Contrary to expectations of a strong influence of IS therapy on the immunoreactivity, this study showed only minor differences between the groups with high-level, low-level, and no IS. Particularly, the in vitro reactivity to adenovirus antigen was nearly the same in all three groups. We assume that—provided a normal distribution and count of lymphocyte subgroups—patients with moderate immunosuppression might be capable of raising an effective immune response to inactivated and live vaccines.
The prevalence of RLS in pregnancy is higher when compared with the general population however it remains unknown among indigenous black Africans. Available data indicate that RLS is uncommon in sub-Saharan Africa. We embarked on this study to determine the prevalence and characteristics of RLS in an antenatal clinic sample of Nigerian pregnant women compared with a primary care sample of non-pregnant women.
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Cell-lines formed from an individual's tumor can be used to predict response to specific therapies and determine genomic predictors. For mesothelioma, where chemotherapy remains the backbone of current therapeutic paradigms, such assays could be used to treat patients with the most effective agents specific to their "chemical profile".
Purpose: Pulmonary carcinoid tumors account for up to 5% of all lung malignancies in adults, comprise 30% of all carcinoid malignancies, and are defined histologically as typical carcinoid (TC) and atypical carcinoid (AC) tumors. The role of specific genomic alterations in the pathogenesis of pulmonary carcinoid tumors remains poorly understood. We sought to identify genomic alterations and pathways that are deregulated in these tumors to find novel therapeutic targets for pulmonary carcinoid tumors. Experimental Design: We performed integrated genomic analysis of carcinoid tumors comprising whole genome and exome sequencing, mRNA expression profiling and SNP genotyping of specimens from normal lung, typical and atypical carcinoid, and small cell lung carcinoma (SCLC) to fully represent the lung neuroendocrine tumor spectrum. Results: Analysis of sequencing data found recurrent mutations in cancer genes including ATP1A2, CNNM1, MACF1, RAB38, NF1, RAD51C, TAF1L, EPHB2, POLR3B and AGFG1. The mutated genes are involved in biological processes including cellular metabolism, cell division cycle, cell death and apoptosis and immune regulation. The top most significantly mutated genes were TMEM41B, DEFB127, WDYHV1 and TBPL1. Pathway analysis of significantly mutated and cancer driver genes implicated MAPK/ERK and amyloid beta precursor protein (APP) pathways whereas analysis of CNV and gene expression data suggested deregulation of the NF-ĸB and MAPK/ERK pathways. The mutation signature was predominantly C>T and T>C transitions with a minor contribution of T>G transversions. Conclusions: This study identified mutated genes affecting cancer relevant pathways and biological processes that could provide opportunities for developing targeted therapies for pulmonary carcinoid tumors.
Purpose: The classification of medulloblastoma into WNT, SHH, Group 3 and Group 4 subgroups has become of critical importance for patient risk-stratification and subgroup-tailored clinical trials. Here, we aimed to develop a simplified, clinically applicable classification approach that can be implemented in the majority of centers treating patients with medulloblastoma. Experimental Design: We analyzed 1,577 samples comprising previously published DNA methylation microarray data (913 medulloblastomas, 457 non-medulloblastoma tumors, 85 normal tissues), and 122 frozen and formalin-fixed paraffin-embedded medulloblastoma samples. Biomarkers were identified applying stringent selection filters and Linear Discriminant Analysis (LDA) method, and validated using DNA methylation microarray data, bisulfite pyrosequencing and direct-bisulfite sequencing. Results: Using a LDA-based approach, we developed and validated a prediction method (EpiWNT-SHH classifier) based on six epigenetic biomarkers that allowed for rapid classification of medulloblastoma into the clinically relevant subgroups WNT, SHH and non-WNT/non-SHH with excellent concordance (>99%) with current gold-standard methods, DNA methylation microarray and gene-signature profiling analysis. The EpiWNT-SHH classifier showed high prediction capacity using both frozen and formalin-fixed material, as well as diverse DNA methylation detection methods. Similarly, we developed a classifier specific for Group 3 and Group 4 tumors, based on five biomarkers (EpiG3-G4) with good discriminatory capacity, allowing for correct assignment of more than 92% of tumors. EpiWNT-SHH and EpiG3-G4 methylation profiles remained stable across tumor primary, metastasis and relapse samples. Conclusions: The EpiWNT-SHH and EpiG3-G4 classifiers represent a new simplified approach for accurate, rapid and cost-effective molecular classification of single medulloblastoma DNA samples, using clinically applicable DNA methylation detection methods.
Purpose: In many children with cancer and characteristics suggestive of a genetic predisposition syndrome, the genetic cause is still unknown. We studied the yield of pathogenic mutations by applying whole exome sequencing on a selected cohort of children with cancer. Experimental design: To identify mutations in known and novel cancer predisposing genes, we performed trio-based whole exome sequencing on germline DNA of 40 selected children and their parents. These children were diagnosed with cancer and had at least one of the following features: (1) intellectual disability and/or congenital anomalies, (2) multiple malignancies, (3) family history of cancer or (4) an adult type of cancer. We first analyzed the sequence data for germline mutations in 146 known cancer predisposing genes. If no causative mutation was found, the analysis was extended to the whole exome. Results: Four patients carried causative mutations in a known cancer predisposing gene: TP53 and DICER1 (n=3). In another four patients, exome sequencing revealed mutations causing syndromes that might have contributed to the malignancy (EP300-based Rubinstein-Taybi syndrome, ARID1A-based Coffin-Siris syndrome, ACTB-based Baraitser-Winter syndrome and EZH2-based Weaver syndrome). In addition, we identified two genes, KDM3B and TYK2, which are possibly involved in genetic cancer predisposition. Conclusion: In our selected cohort of patients, pathogenic germline mutations causative or likely causative of the cancer phenotype were found in eight patients and two possible novel cancer predisposing genes were identified. Therewith, our study shows the added value of sequencing beyond a cancer gene panel in selected patients, to recognize childhood cancer predisposition.
Purpose: Ovarian carcinoma no longer responsive to surgery and chemotherapy remains an incurable disease. Alternative therapeutic options remain desperately needed. Experimental Design: We describe a heavily pretreated ovarian cancer patient with recurrent disease experiencing a remarkable clinical response to treatment with the anti-PD1 immune check-point inhibitor pembrolizumab. The clinical, pathological, and genomic characteristics of this exceptional ovarian cancer responder were carefully investigated using immunohistochemistry (IHC), quantitative multiplex fluorescence methods (ie, automated quantitative analysis, AQUA) and whole exome sequencing (WES) techniques. Results: The patient harbored a recurrent/metastatic radiation and chemotherapy-resistant high grade ovarian carcinoma with clear cell features. While progressing on any standard treatment modality she demonstrated a remarkable complete response to the anti-PD1 immune check-point inhibitor pembrolizumab. WES results were notable for the presence a relative low number of mutations (Tumor Mutation Load/Mb = 4.31, total mutations = 164) and a peculiar structural variant disrupting the 3' region of the PD-1L gene causing aberrant PD-L1 surface expression as confirmed by immunohistochemistry (IHC) and AQUA technology. Heavy infiltration of the PD-L1-mutated and PD-L1-overexpressing tumor with T cell lymphocytes (ie, CD4+/CD8+ TIL), CD68+ macrophages and CD20+ B cells was detected in the surgical specimen strongly suggesting immune evasion as a key mechanism of tumor growth and survival. Patient's complete clinical responses remain unchanged at the time of the writing of this report with no significant side-effects reported to date. Conclusions: Anti-PD1 inhibitors may represent a novel treatment option for recurrent/metastatic human tumors refractory to salvage treatment harboring PD-L1 gene structural variations causing aberrant PD-L1 expression.
Hyperactivation of the NFκB pathway is a distinct feature of inflammatory breast cancer (IBC), a highly proliferative and lethal disease. Gene expression studies in IBC patient tissue have linked epidermal growth factor receptor (EGFR/HER2)-mediated MAPK signaling to NFκB hyperactivity, but the mechanism(s) by which this occurs remain unclear. Here, we report that the X-linked inhibitor of apoptosis protein (XIAP) plays a central role in linking these two pathways. XIAP overexpression correlated with poor prognoses in breast cancer patients and was frequently observed in untreated IBC patient primary tumors. XIAP drove constitutive NFκB transcriptional activity, which mediated ALDH positivity (a marker of stem-like cells), in vivo tumor growth, and an IBC expression signature in patient-derived IBC cells. Using pathway inhibitors and mathematical models, we defined a new role for the MAPK-interacting (Ser/Thr)-kinase (MNK) in enhancing XIAP expression and downstream NFκB signaling. Furthermore, targeted XIAP knockdown and treatment with a MNK inhibitor decreased tumor cell migration in a dorsal skin fold window chamber murine model that allowed for intra-vital imaging of local tumor growth and migration. Together, our results indicate a novel role for XIAP in the molecular crosstalk between MAPK and NFκB pathways in aggressive tumor growth, which has the potential to be therapeutically exploited.
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Previous genome-wide association studies (GWAS) have identified several common genetic variants that may significantly modulate cancer susceptibility. However, the precise molecular mechanisms behind these associations remain largely unknown; it is often not clear whether discovered variants are themselves functional or merely genetically linked to other functional variants. Here we provide an integrated method for identifying functional regulatory variants associated with cancer and their target genes by combining analyses of expression quantitative trait loci (eQTL), a modified version of allele-specific expression (ASE) that systematically utilizes haplotype information, transcription factor (TF) binding preference, and epigenetic information. Application of our method to a breast cancer susceptibility region in 5p12 demonstrates that the risk allele rs4415084-T correlates with higher expression levels of the protein-coding gene mitochondrial ribosomal protein S30 (MRPS30) and lncRNA RP11-53O19.1. We propose an intergenic SNP rs4321755, in linkage disequilibrium (LD) with the GWAS SNP rs4415084 (r2=0.988), to be the predicted functional SNP. The risk allele rs4321755-T, in phase with the GWAS rs4415084-T, created a GATA3 binding motif within an enhancer, resulting in differential GATA3 binding and chromatin accessibility, thereby promoting transcription of MRPS30 and RP11-53O19.1. MRPS30 encodes a member of the mitochondrial ribosomal proteins, implicating the role of risk SNP in modulating mitochondrial activities in breast cancer. Our computational framework provides an effective means to integrate GWAS results with high-throughput genomic and epigenomic data and can be extended to facilitate rapid functional characterization of other genetic variants modulating cancer susceptibility.
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Although ribosomal protein S6 kinase A3 (RSK) activation status positively correlates with patient responses to anti-estrogen hormonal therapies, the mechanistic basis for these observations is unknown. Using multiple in vitro and in vivo models of ER+ breast cancer, we report that ERα sequesters active RSK2 into the nucleus to promote neoplastic transformation and facilitate metastatic tumor growth. RSK2 physically interacted with ERα through its N-terminus to activate a pro-neoplastic transcriptional network critical to the ER+ lineage in the mammary gland, thereby providing a gene signature that effectively stratified patient tumors according to ERα status. ER+ tumor growth was strongly dependent on nuclear RSK2, and transgenic mice engineered to stably express nuclear RSK2 in the mammary gland developed high grade ductal carcinoma in situ. Mammary cells isolated from the transgenic model and introduced systemically successfully disseminated and established metastatic lesions. Anti-estrogens disrupted the interaction between RSK2 and ERα, driving RSK2 into the cytoplasm and impairing tumor formation. These findings establish RSK2 as an obligate participant of ERα-mediated transcriptional programs, tumorigenesis, and divergent patient responses to anti-estrogen therapies.
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Although obesity with associated inflammation is now recognized as a risk factor for breast cancer and distant metastases, the functional basis for these connections remain poorly understood. Here we show that in breast cancer patients and in animal breast cancer models, obesity is a sufficient cause for increased expression of the bioactive sphingolipid mediator sphingosine-1-phosphate (S1P) which mediates cancer pathogenesis. A high fat diet was sufficient to upregulate expression of sphingosine kinase 1 (SphK1), the enzyme that produces S1P, along with its receptor S1PR1 in syngeneic and spontaneous breast tumors. Targeting the SphK1/S1P/S1PR1 axis with FTY720/fingolimod attenuated key pro-inflammatory cytokines, macrophage infiltration and tumor progression induced by obesity. S1P produced in the lung pre-metastatic niche by tumor-induced SphK1 increased macrophage recruitment into the lung and induced IL-6 and signaling pathways important for lung metastatic colonization. Conversely, FTY720 suppressed IL-6, macrophage infiltration and S1P-mediated signaling pathways in the lung induced by a high fat diet, and it dramatically reduced formation of metastatic foci. In tumor-bearing mice, FTY720 similarly reduced obesity-related inflammation, S1P signaling and pulmonary metastasis, thereby prolonging survival. Taken together, our results establish a critical role for circulating S1P produced by tumors and the SphK1/S1P/S1PR1 axis in obesity-related inflammation, formation of lung metastatic niches and breast cancer metastasis, with potential implications for prevention and treatment.
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Publication date: May 2018
Source:Computer Speech & Language, Volume 49
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Progestogen hypersensitivity (PH) is a rare disorder which usually occurs in women of childbearing age with symptoms ranging from urticaria with or without angioedema, multiple organ involvement consistent with allergic anaphylaxis, to a spectrum of other non-evanescent skin eruptions. In this review, we present a clinical vignette of PH and discuss the clinical presentation and proposed pathomechanisms, diagnosis, and treatment of PH.
The hypersensitivity symptoms are associated with exogenous progestin exposure (e.g., contraceptive medicines, in vitro fertilization therapy) or endogenous progesterone from progesterone surges during the luteal phase of the menstrual cycle and pregnancy. Recognition of this condition can be challenging to the clinician due to its heterogeneous clinical presentation. It has been recently proposed to use the new term "progestogen hypersensitivity" to replace "autoimmune progesterone dermatitis" due to the lack of evidence supporting an autoimmune mechanism for this disorder. In addition, diagnostic and treatment algorithms are now available that can lead to successful management of this condition. More new developments of Progesterone desensitization protocols are now available which appear to be the safest and most effective long-term treatment option for PH.
With the extensive use of oral contraceptives and increased use of supra-physiologic doses of progesterone to support pregnancy in in vitro fertilization, there is likely to be a higher prevalence of PH in the future than currently recognized. Therefore, the allergist-immunologist will be required to collaborate with gynecologists and reproductive endocrinologists to diagnose and treat this condition.
Primary familial brain calcification (PFBC) is a rare disorder characterized by distinctive bilateral brain calcification and variable clinical presentations. However, cerebrovascular attack was rarely reporte...
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Sensory impairment hinders a person's ability to interact with their environment, and thus reduces their quality of life. In the case of impaired somatosensory perception, visual input can only provide indirect information at non-negligible cognitive cost. Therefore, restoration of natural somatosensory perception via artificial means has led to the exploration of different biological targets (Weber et al., 2012). Stimulation of the somatosensory cortex (Bensmaia, 2015), dorsal root ganglia (Weber et al., 2011), and peripheral nerves (Pasluosta et al., 2018) can produce intuitive and near-natural tactile and proprioceptive sensations, although proprioception has been studied to a lesser extent than touch (Weber et al., 2012).
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Pathophysiological descriptions of amyotrophic lateral sclerosis (ALS) have broadened in recent years to include recognition of widespread involvement of brain pathways in the 'connectome', including corpus callosum, with degenerative neuronal pathology in associated cortical areas, basal ganglia, brainstem, cerebellum and spinal cord. In general, these pathological changes are in the anterior brain and its connections, and thus in the classical motor and also in the emotionally expressive brain, including frontal lobes anterior to primary motor areas and temporal lobes.
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The abdominal wall does not comprise a distinct organ, and is often cursorily evaluated on CT. However, it is affected by many different pathological processes. These may be categorized according to their underlying etiology - trauma, infection or inflammation, iatrogenic and neoplastic process - or according to the abdominal wall layer they affect. We chose instead to group these lesions into six distinct categories based on their CT characteristic density: solid, infiltrative, hypervascular, fluid, fat, and bone density lesions.
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J Neurol Surg B
DOI: 10.1055/s-0037-1617432
Objectives/Hypothesis The endoscopic endonasal approach (EEA) for nasopharyngectomy is an alternative to the maxillary swing approach (MSA) for selected recurrent nasopharyngeal carcinomas (NPC). We compare the access between these approaches. Methods Three cadaver specimens were used to compare access volumes of the EEA and MSA. Exposure volumes were calculated using image guidance registration to cone beam computed tomography and tracking of accessible tissue with volumetric quantification. The area of exposure to the carotid artery was measured. Results The MSA provided higher volumes for access volume compared with the EEA (66.6 vs 39.1 cm3, p = 0.009). The working area was larger in the MSA (80.2 vs 56.9 cm2, p = 0.06). The exposure to the carotid artery was higher in the MSA (1.88 vs 1.62 cm2, p = 0.04). The MSA provided larger volume of exposure for tumors of the parapharyngeal space with exposure below the palate. Conclusions This study suggests that the MSA for nasopharyngectomy provides a larger volume of exposure. However, much of the increased exposure relates to exposure of the parapharyngeal space below the palate. The EEA provides adequate access to superior anatomical structures.
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Georg Thieme Verlag KG Stuttgart · New York
Article in Thieme eJournals:
Table of contents | Abstract | Full text
J Neurol Surg B
DOI: 10.1055/s-0037-1620247
Georg Thieme Verlag KG Stuttgart · New York
Article in Thieme eJournals:
Table of contents | Full text
J Neurol Surg B
DOI: 10.1055/s-0037-1618577
Background The assessment of pituitary tumor (PT) volume is important in the treatment and follow-up of patients with PT. Previously, PT volume estimation has been performed by conventional geometric equations (CGE) such as abc/2 (simplified ellipsoid volume equation) and 4πr3/3 (sphere), both presuming a symmetric tumor shape, which occurs uncommonly in patients with PT. In contrast, three-dimensional (3D) voxel-based software segmentation takes the irregular and asymmetric shapes that PTs often possess into account and might be a more accurate method for PT volume segmentation.The purpose of this study is twofold. (1) To compare 3D segmentation with CGE for PT volume estimation. (2) To assess inter-rater reliability in 3D segmentation of PTs. Methods Nineteen high-resolution (1mm slice thickness) T1-weighted MRI examinations of patients with PT were independently analyzed and manually segmented, using the software ITK-SNAP, by two certified neuroradiologists. Concurrently, the volumes of the PTs were estimated with abc/2 and 4πr3/3 by a clinician, and the results were compared with the corresponding segmented volumes. Results There was a significant decrease in PT volume attained from the segmentations compared with the calculations made with abc/2 (p < 0.001, mean volume 18% higher than segmentation) and 4πr3/3 (p < 0.001, mean volume 28% higher than segmentation). The intraclass correlation coefficient (ICC) for the two sets of segmented PTs was 0.99. Conclusion CGE (abc/2 and 4πr3/3) significantly overestimates PT volume compared with 3D volumetric segmentation. The inter-rater agreement on manual 3D volumetric software segmentation is excellent.
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Georg Thieme Verlag KG Stuttgart · New York
Article in Thieme eJournals:
Table of contents | Abstract | Full text
J Neurol Surg B
DOI: 10.1055/s-0037-1621738
Pediatric craniopharyngioma is a rare sellar-region epithelial tumor that, in spite of its typically benign pathology, has the potential to be clinically devastating, and presents a host of formidable management challenges for the skull base surgeon. Strategies in craniopharyngioma care have been the cause of considerable controversy, with respect to both philosophical and technical issues. Key questions remain unresolved, and include optimizing extent-of-resection goals; the ideal radiation modality and its role as an alternative, adjuvant, or salvage treatment; appropriate indications for expanded endoscopic endonasal surgery as an alternative to transcranial microsurgery; risks and benefits of skull base techniques in a pediatric population; benefits of and indications for intracavitary therapies; and the preferred management of common treatment complications. Correspondingly, we sought to review the preceding basic science and clinical outcomes literature on pediatric craniopharyngioma, so as to synthesize overarching recommendations, highlight major points of evidence and their conflicts, and assemble a general algorithm for skull base surgeons to use in tailoring treatment plans to the individual patient, tumor, and clinical course. In general terms, we concluded that safe, maximal, hypothalamic-sparing resection provides very good tumor control while minimizing severe deficits. Endoscopic endonasal, intraventricular, and transcranial skull base technique all have clear roles in the armamentarium, alongside standard craniotomies; these roles frequently overlap, and may be further optimized by using the approaches in adaptive combinations. Where aggressive subtotal resection is achieved, patients should be closely followed, with radiation initiated at the time of progression or recurrence—ideally via proton beam therapy, although three-dimensional conformal radiotherapy, intensity-modulated radiotherapy, and stereotactic radiosurgery are very appropriate in a range of circumstances, governed by access, patient age, disease architecture, and character of the recurrence. Perhaps most importantly, outcomes appear to be optimized by consolidated, multidisciplinary care. As such, we recommend treatment in highly experienced centers wherever possible, and emphasize the importance of longitudinal follow-up—particularly given the high incidence of recurrences and complications in a benign disease that effects a young patient population at risk of severe morbidity from hypothalamic or pituitary injury in childhood.
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Georg Thieme Verlag KG Stuttgart · New York
Article in Thieme eJournals:
Table of contents | Abstract | Full text
J Neurol Surg B
DOI: 10.1055/s-0038-1623520
Unilateral suprasellar meningiomas have distinct features compared to other midline tumors, as they may produce severe visual symptoms even if small due to an early involvement of the optic canal. Surgical treatment of these tumors from an ipsilateral approach is challenging, as the tumor is covered by the optic nerve that needs to be mobilized to access the optic canal extension. A contralateral approach allows a direct line of sight to the tumor despite a longer working distance. We report the case of a 49-year-old patient presenting with unilateral visual loss related to a left suprasellar meningioma extending to the left optic canal and displacing the optic nerve laterally. Through a right eyebrow approach, a 2.5/2 cm supraorbital bone flap was raised and the orbital floor was thoroughly flattened. After dural opening, the carotid cistern was opened and CSF evacuated allowing a surgery without fixed retractors. The intracranial part of the tumor was removed, but the optic nerve seemed to be still displaced by the intracanalicular part. Under copious irrigation, the medial part of the optic canal was drilled, the dura incised, and the tumor removed. Postoperative course was favorable and the patient made a complete visual recovery. Postoperative MRI showed complete removal of the tumor. We present different surgical steps and discuss the nuances of the procedure. The contralateral eyebrow approach is an interesting addition to the surgical armamentarium and should be discussed for unilateral suprasellar tumors.The link to the video can be found at: https://youtu.be/2LTEOaGoKzo.
[...]
Georg Thieme Verlag KG Stuttgart · New York
Article in Thieme eJournals:
Table of contents | Abstract | open access Full text