Early Postoperative Complications in Meningioma: Predictive Factors and Impact on Outcome

BACKGROUND: Craniotomies carry inherent risks of postoperative complications that may have a negative impact on patients\u27 status. Recognizing and preventing surgical complications is of paramount importance, especially in meningioma surgery, where most of these tumors are benign and current management protocols are effective in terms of disease control and maintenance of higher quality of life. The objective of this study was to describe the early complications after surgery and their predictive factors in patients undergoing resection of intracranial meningiomas. METHODS: A partly retrospective, partly prospective review was conducted in a Norwegian population-based cohort of 1469 consecutive cases of meningioma surgery treated at the university hospitals of Oslo, totaling 11,414 patient-years of follow-up. RESULTS: 2.6% of patients had a postoperative hematoma, 2.7% a postoperative infection, 3.9% a postoperative worsening of neurologic status; 5.4% of patients died during a 30-day period after surgery. Predictive factors of increased risk of postoperative complications were patient\u27s age for the hematoma, a non-skull base meningioma for infection, and postoperative hematoma for the risk of neurologic worsening or 30-day mortality. CONCLUSIONS: Early postoperative complications in meningioma surgery have a negative impact on patient survival and postoperative neurologic status, in a disease where survival is usually not limited by the meningioma itself. In this study, we identified risk factors for early postoperative complications, the identification of at-risk populations may help to prevent the occurrence of these risk factors

Posterior fossa meningiomas: perioperative predictors of extent of resection, overall survival and progression-free survival

BACKGROUND: Posterior fossa meningiomas (PFMs) often represent surgical challenges due to their proximity to neurovascular structures. Factors predicting the extent of resection (EOR), overall survival (OS), and progression-free survival (PFS) were identified and integrated in a prediction tool to offer evidence-based personalized therapeutic strategies. METHODS: All meningiomas managed surgically from 1990 to 2010 from a single-center were reviewed. A classification tree was created using the classification and regression tree recursive partitioning analysis that incorporated patient and tumor data available before surgery in order to predict the rates of gross total resection (GTR). RESULTS: A total of 198 patients were identified (female-to-male ratio, 2.7; mean age, 59.1 years) and compared with 1271 supratentorial meningiomas (STMs) operated in the same institution during the same time period. GTR was achieved less often (59.6% versus 81.9%; p < 0.01) in PFMs than STMs. Preoperative neurological symptoms were predictive of higher Simpson grades (OR, 2.19 [1.05; 4.58]; p = 0.04). Age was associated with reduced OS (OR, 1.08 [1.04;1.12]; p < 0.001). A KPS ≥ 70 was associated with higher survival rates (OR, 2.70 [2.19;2.92]; p = 0.02). Higher WHO grades were associated with reduced OS (OR, 3.56 [1.02;12.47]; p = 0.05). The GTR rate varies from 80% in patients without a preoperative deficit to 40% patients with a preoperative deficit, younger than 60 years old, and with adjacent bone invasion. CONCLUSIONS: This study provides a classification tree of the predictors of EOR in PFMs, based upon preoperative demographic, clinical, and radiological variables. An evidence-based management protocol with estimated EORs may guide the decision-making process in PFMs

Association of Medical Comorbidities With Objective Functional Impairment in Lumbar Degenerative Disc Disease

STUDY DESIGN Analysis of a prospective 2-center database. OBJECTIVES Medical comorbidities co-determine clinical outcome. Objective functional impairment (OFI) provides a supplementary dimension of patient assessment. We set out to study whether comorbidities are associated with the presence and degree of OFI in this patient population. METHODS Patients with degenerative diseases of the spine preoperatively performed the timed-up-and-go (TUG) test and a battery of questionnaires. Comorbidities were quantified using the Charlson Comorbidity Index (CCI) and the American Society of Anesthesiology (ASA) grading. Crude and adjusted linear regression models were fitted. RESULTS Of 375 included patients, 97 (25.9%) presented at least some degree of medical comorbidity according to the CCI, and 312 (83.2%) according to ASA grading. In the univariate analysis, the CCI was inconsistently associated with OFI. Only patients with low-grade CCI comorbidity displayed significantly higher TUG test times (p = 0.004). In the multivariable analysis, this effect persisted for patients with CCI = 1 (p = 0.030). Regarding ASA grade, patients with ASA = 3 exhibited significantly increased TUG test times (p = 0.003) and t-scores (p = 0.015). This effect disappeared after multivariable adjustment (p = 0.786 and p = 0.969). In addition, subjective functional impairment according to ODI, and EQ5D index was moderately associated with comorbidities according to ASA (all p < 0.05). CONCLUSION The degree of medical comorbidities appears only weakly and inconsistently associated with OFI in patients scheduled for degenerative lumbar spine surgery, especially after controlling for potential confounders. TUG testing may be valid even in patients with relatively severe comorbidities who are able to complete the test

WHO grade I meningiomas: classification-tree for prognostic factors of survival

World Health Organization (WHO) grade I meningiomas are intracranial extracerebral tumors, in which microsurgery as a stand-alone therapy provides high rates of disease control and low recurrence rates. Our aim was to identify prognostic factors of overall survival and time-to-retreat (OS; TTR) in a cohort of patients with surgically managed WHO grade I meningioma. Patients with WHO grade I meningiomas from a retrospectively (1990 to 2002) and prospectively managed (2003 to 2010) databank of Oslo University Hospital, Norway, were included. The mean follow-up was 9.2 ± 5.7 years, with a total of 11,414 patient-years. One thousand three hundred fifty-five patients were included. The mean age was 58 ± 13.2, mean Karnofsky Performance Status (KPS) 92.6 ± 26.1 and female-to-male ratio 2.5:1. The 1-year, 5-year, 10-year, 15-year, and 20-year probabilities were 0.98, 0.91, 0.87, 0.84, and 0.8 for TTR. Patient age (OR 0.92 [0.91, 0.94]), male sex (OR 0.59 [0.45, 0.76]), preoperative KPS ≥ 70 (OR 2.22 [1.59, 3.13]), skull base location (OR 0.77 [0.60, 1]), and the occurrence of a postoperative hematoma (OR 0.44 [0.26, 0.76]) were identified as independent prognostic factors of OS. Patient age (OR 1.02 [1.01, 1.03]) and skull base location (OR 0.30 [0.21, 0.45]) were independent predictors of decreased PFS. Using a recursive partitioning analysis, we suggest a classification tree for the prediction of 5-year PFS based on patient and tumor characteristics. The findings from this cohort of meningioma WHO I patients helps to identify patients at risk of recurrence and tailor the therapeutic management

Incidental durotomy in lumbar spine surgery—a three-nation survey to evaluate its management

Background: Although it is generally accepted that incidental durotomies (ID) should be primarily repaired, the current literature shows no consensus regarding the peri- and postoperative management in case of ID during lumbar spine surgery. Because ID is a rather frequent complication and may be associated with significant disability, we were interested to analyze the current handling of ID in three European countries. Methods: In March 2014, members of the Swiss, German, and Austrian neurosurgical and spine societies were asked to complete an online questionnaire regarding the management of ID during and after lumbar spine surgery. Two, respectively 4weeks after the first invitation, reminder requests were sent to all invitees, who had not already responded at that time. Results: There were 175 responses from 397 requests (44.1%). Responders were predominantly neurosurgeons (89.7%; 10.3% were orthopedic surgeons), of which 45.7, 40.0, and 17.8% work in a non-university hospital, university hospital, and private clinic, respectively. As for the perioperative management of ID, 19.4% of the responders suggest only bed rest, while, depending on the extent of the ID, 84.0% suggest additional actions, TachoSil/Spongostan with fibrin glue or a similar product and single suture repair being the most mentioned. Concerning epidural wound drainage in case of ID, 37.2% desist from placing an epidural wound drainage with or without aspiration, 30.9% place it sometimes, and 33.7% place it regularly, but only without aspiration. Most responders prescribe bed rest for 24 (34.9%) or 48h (28.0%), with much fewer prescribing bed rest for 72h (6.3%) and none more than 72h, and 14.9% of participants never prescribe bed rest. The vast majority of physicians (82.9%, n = 145) always inform their patients after the operation in case of ID. Conclusions: There is substantial heterogeneity in the management of incidental durotomies. The majority of spine surgeons today aim at complete/sufficient primary repair of the ID with varying recommendations concerning postoperative bed rest. Still, there is a trend towards early mobilization if the incidental durotomy has been closed completely/sufficiently with no participant favoring bed rest for more than 72h

Zinc deficiency and neurodevelopment: the case of neurons

Zinc is essential for normal brain development. Gestational severe zinc deficiency can lead to overt fetal brain malformations. Although not teratogenic, suboptimal zinc nutrition during gestation can have long-term effects on the offspring's nervous system. This article will review current knowledge on the role of zinc in modulating neurogenesis and neuronal apoptosis as well as the proposed underlying mechanisms. A decrease in neuronal zinc causes cell cycle arrest, which in part involves a deregulation of select signals (ERK1/2, p53, and NF-κB). Zinc deficiency also induces apoptotic neuronal death through the intrinsic (mitochondrial) pathway, which can be triggered by the activation of the zinc-regulated enzyme caspase-3, and as a consequence of abnormal regulation of prosurvival signals (ERK1/2 and NF-κB). Alterations in the finely tuned processes of neurogenesis, neuronal migration, differentiation, and apoptosis, which involve the developmental shaping of the nervous system, could have a long-term impact on brain health. Zinc deficiency during gestation, even at the marginal levels observed in human populations, could increase the risk for behavioral/neurological disorders in infancy, adolescence, and adulthood.Fil: Adamo, Ana María. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Química y Físico-Química Biológicas "Prof. Alejandro C. Paladini". Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Química y Físico-Química Biológicas; ArgentinaFil: Oteiza, Patricia Isabel. University of California at Davis; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

The Role of Zinc in the Modulation of Neuronal Proliferation and Apoptosis

Although a requirement of zinc (Zn) for normal brain development is well documented, the extent to which Zn can modulate neuronal proliferation and apoptosis is not clear. Thus, we investigated the role of Zn in the regulation of these two critical events. A low Zn availability leads to decreased cell viability in human neuroblastoma IMR-32 cells and primary cultures of rat cortical neurons. This occurs in part as a consequence of decreased cell proliferation and increased apoptotic cell death. In IMR-32 cells, Zn deficiency led to the inhibition of cell proliferation through the arrest of the cell cycle at the G0/G1 phase. Zn deficiency induced apoptosis in both proliferating and quiescent neuronal cells via the intrinsic apoptotic pathway. Reductions in cellular Zn triggered a translocation of the pro-apoptotic protein Bad to the mitochondria, cytochrome c release, and caspase-3 activation. Apoptosis is the resultant of the inhibition of the prosurvival extracellular-signal-regulated kinase, the inhibition of nuclear factor-kappa B, and associated decreased expression of antiapoptotic proteins, and to a direct activation of caspase-3. A deficit of Zn during critical developmental periods can have persistent effects on brain function secondary to a deregulation of neuronal proliferation and apoptosis