Aim of this paper is to recall the surgical technique used in the recurrent lumbar disc herniations (LDHs) and to share our experiences.Out of series of 1115 patients who underwent operations for LDH between 2006 and 2013, 70 patients underwent re-operations, which were included in this study. During surgery, lateral decompression performed over the medial facet joint to the superior facet joint border was seen after widening the laminectomy defect, and microdiscectomy was performed. The demographic findings of the patients, their complaints in admission to hospital, the level of operation, the condition of dural injury, the first admission in the prospective analysis, and their quality of life were evaluated through the Oswestry scoring during their postoperative 1(st), 3(rd), 6(th)-month and 1(st), 3(rd), 5(th) and 7(th)-year follow-up. In the statical analysis, Friedman test was performed for the comparison of the Oswestry scores and Siegel Castellan test was used for the paired nonparametrical data. A P < 0.05 was considered statistically significant.Considering the Oswestry Index during the follow-ups, the values in the postoperative early period and follow-ups were seen to be significantly lower than those at the time of admission to hospital (P < 0.05). None of the patients, who re-operated by microdiscectomy, presented with iatrogenic instability in 7 years follow-up period.Microdiscectomy performed through a proper technique in the re-operation of recurrent disc herniations eases complaints and improves the quality of life. Long-term follow-ups are required for more accurate results.
<b><i>Background/Aim:</i></b> There is currently no objective evaluation of hearing in patients with hydrocephalus (HCP), and we could not find any study in the literature comprising a sufficient number of patients with a high level of scientific evidence. In the current study, we used the auditory brainstem response (ABR) test to assess whether hearing function in patients with HCP is altered after ventriculoperitoneal shunt surgery. <b><i>Methods:</i></b> In total, 20 newborn patients with HCP (13 female, 7 male) were enrolled in this study. For each patient, ABR testing was performed at three time points: 1 day prior to the operation and on days 7 and 90 after the operation. ABRs using click stimuli of 90, 70, 50 and 30 dB nHL (normal hearing level) were achieved for V-wave latency, and I-III and I-IV interpeak latencies for both ears were recorded. Variance analysis for parametric data and Tukey's post hoc honest significant difference test were used to demonstrate the relationship between the results obtained from the different recording periods. Results were considered significant at p < 0.05, and 95% confidence intervals were calculated. <b><i>Results:</i></b> The mean values of the ABR tests were compared between the pre- and postoperative results, which showed an increase (faster transmission) of nerve conduction velocity of 0.2 ms. The results were not statistically significant for 50 and 90 dB (p > 0.05) but were significant for 30 and 70 dB (p < 0.05). <b><i>Conclusion:</i></b> Diagnosis in hydrocephalic patients is important not only for the treatment but also for the prevention of HCP-associated complications. Early treatment appears to be promising in terms of auditory benefit. Prompt diagnosis and treatment are therefore essential as soon as possible.
Computerized tomography and conventional magnetic resonance imaging (MRI) have been used to show many structural alterations that can either develop because of, or accompany, CMI.These include cerebellar tonsillar herniation, small posterior fossa volume, basilar invagination, occipitalization of the atlas, hydrocephalus, and syringomyelia (4,9,15).In addition, many specific morphometric findings have been reported, such as a shallow posterior cranial fossa, short anteroposterior length of the foramen magnum, and a large angle of the tentorium (4).Although correlations have been confirmed between these structural alterations and clinical presentations in various studies, the degree of tonsillar herniation has not always been compatible with the █ INTRODUCTION T ype 1 Chiari malformation (CMI) is the most common Chiari malformation, and is characterized by caudal displacement of the cerebellar tonsils into the cervical canal through the foramen magnum.The clinical signs and symptoms of CMI are believed to be manifestations of these anatomical changes.Consistent with this, patients with CMI exhibit various clinical signs and symptoms, due to cerebellar signs, brainstem compression, cranial nerve dysfunction, and spinal cord injury.Prominent examples include head, neck, back, and limb pain, as well as limb movement disorders, spasticity, sensory disturbances, vertigo, ataxia, nystagmus, and dysphagia (5,9,16).AIM: To evaluate the preoperative and postoperative 6 th month mean apparent diffusion coefficient (ADC) values of the cerebellar tonsils and bulbus in patients with Chiari Malformation Type I (CMI), and to compare the results with healthy controls. MATERIAL and METHODS:We included 15 patients with CMI who underwent suboccipital decompression, upper cervical laminectomy, and duraplasty surgery, and compared them with 10 healthy individuals.Three regions of interest were placed, one each in the cerebellar tonsils and one in the bulbus.The mean ADC values were measured separately in each region.RESULTS: Among the patients, mean ADC values were significantly decreased after surgery compared with before surgery.The mean ADC values before surgery were significantly higher for patients than for controls; however, although the mean ADC values were slightly higher after surgery for patients than for controls, the differences were not significant.Thus, after surgical intervention, ADC values in patients with CMI became close to those of normal individuals. CONCLUSION:The increased ADC values in patients with CMI before surgery implied that not only morphologic changes but also increased diffusivity may play a key role in the pathophysiology and clinical presentation of the disease.Decompression surgery can produce favorable diffusional alterations.
It has been universally believed that spindle assembly checkpoint (SAC) proteins which include the kinetochore proteins are involved in monitoring the faithful segregation of sister chromatids during cell division and hence defects in these proteins result in anueploidy. Furthermore, there are multiple sources of experimental data to suggest that a defect in p53 could also promote genomic instability leading to anueploidy. Despite these observations, a molecular basis for the prevention of aneuploidy to maintain genomic integrity upon activation of SAC has largely remained elusive. In this report, we demonstrate a novel mechanism for the maintenance of a balance between cell survival and apoptosis upon activation of SAC. We found that depletion of the outer kinetochore protein hBub1 upon activation of SAC primarily triggers early cell death mediated by p53. This phenomenon is further supported by the up-regulation of p53 down-stream pro-apoptotic genes, BAX and PUMA as well as a corresponding increase in the cleavage products of PARP and caspase 3, markers of apoptosis upon depletion of hBub1 in SAC activated cells. On the other hand, as expected, concomitant loss of both hBub1 and p53 resulted in disabling of the p53 mediated cell death pathway leading to the accumulation of cells with aneuploidy/polyploidy.Commentary also to:hBub1 negatively regulates p53 mediated early cell death upon mitotic checkpoint activationFangming Gao, Jose F Ponte, Panagiotis Papageorgis, Mary Levy, Sait Ozturk, Arthur W. Lambert, Arunthathi Thiagalingam, Hamid Mostafavi Abdolmaleky, Beth A Sullivan and Sam Thiagalingam
Menengiomlar kanlanmasi yogun tumorlerdir. Ozellikle buyuk boyutlarda olan pial/kortikal invazyon yapan menengiomlarin cerrahisi iskemik ve/veya hemorajik komplikasyonlar icerebilir. 49 yasinda erkek hasta, basagrisi ve sol vucut yarisinda gucsuzluk nedeniyle basvurdu. Beyin manyetik rezonans goruntulemede (MRG) sag frontopariyetelde saptanan menengiom nedeniyle opere edildi. Kitle total cikarildi. Kitlenin eksizyonu sonrasi pial damarlardan sizinti seklinde kanamalar mevcuttu. Bu kanama alanlarinin uzerine her biri yaklasik 1x1 cm boyutlarinda 4 adet Surgicel® ortuldu. Hasta 3 hafta sonra sol hemiparezi nedeniyle tekrar basvurdu. Beyin MRG’de cerrahi uygulanan alanda menengiomdan farkli nitelikte, daha kucuk bir lezyon izlendi. Hasta tekrar cerrahiye alindi. Lezyonun absorbe olamamis Surgicel®’lerden olustugu gozlendi ve eksize edildi. Bircok cerrahi bransin hemostaz amacli tercih ettikleri Surgicel®, erken donemde absorbe olabilen bir materyaldir. Ancak nadirende olsa absorbe olamayip kan ile temasi sonrasi ekspanse olabilir. Sonucta Surgicel® kitle etkisi ya da noral yapilar uzerinde basi etkisi yapabilir. Bu durum ozellikle norosirurji ameliyatlarinda akilda tutulmalidir.
Breast cancer progression is associated with aberrant DNA methylation and expression of genes that control the epithelial-mesenchymal transition (EMT), a critical step in malignant conversion. Although the genes affected have been studied, there is little understanding of how aberrant activation of the DNA methylation machinery itself occurs. Using a breast cancer cell-based model system, we found that cells that underwent EMT exhibited overactive transforming growth factor beta (TGFbeta) signaling and loss of expression of the CDH1, CGN, CLDN4, and KLK10 genes as a result of hypermethylation of their corresponding promoter regions. Based on these observations, we hypothesized that activated TGFbeta-Smad signaling provides an "epigenetic memory" to maintain silencing of critical genes. In support of this hypothesis, disrupting Smad signaling in mesenchymal breast cancer cells resulted in DNA demethylation and reexpression of the genes identified. This epigenetic reversal was accompanied by an acquisition of epithelial morphology and a suppression of invasive properties. Notably, disrupting TGFbeta signaling decreased the DNA binding activity of DNA methyltransferase DNMT1, suggesting that failure to maintain methylation of newly synthesized DNA was the likely cause of DNA demethylation. Together, our findings reveal a hyperactive TGFbeta-TGFbetaR-Smad2 signaling axis needed to maintain epigenetic silencing of critical EMT genes and breast cancer progression.
