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Background All brain surgery requires some degree of iatrogenic trauma to healthy tissue. Minimally invasive approaches to brain tumors offer the potential of decreasing this trauma compared with conventional approaches. However, there are no validated radiologic models to examine axonal damage after minimally invasive entry into the brain. Objective To present a cadaveric model of brain cannulation using fractional anisotropy measurements obtained from diffusion tensormagnetic resonance imaging (MRI). Two different methods of access are compared. Methods: Freshly harvested unfixed cadaveric brains were cannulated using both direct and indirect (i.e., dilation followed by cannulation) methods. Specimens were subjected to 68-direction diffusion tensor imaging scans and proton-density imaging. Fractional anisotropy (FA) data froma region of interest surrounding the entry zonewas extracted from scans using imaging software and analyzed. Results: FA values were significantly higher following indirect cannulation (less invasive method) than they were following direct cannulation. FA values for undisturbed brain were significantly higher than in either of the cannulated groups, suggesting an inverse relationship between FA values and brain injury. Conclusion: Axonal damage following brain cannulation can potentially be evaluated by FA analysis in a cadaveric model. These data may lead to an MRI-based model of iatrogenic brain injury following tumor surgery. Future studies will focus on histologic analysis and clinical validation in live tissues. [ABSTRACT FROM AUTHOR]

Background: Spontaneous intracerebral hemorrhages (ICHs) cause significant morbidity and mortality. Traditional open surgical management strategies offer limited benefit except for the most superficial hemorrhages in select patients. Recent reports suggest that endoscopic approaches may improve outcomes, particularly for deep subcortical hemorrhages. However, the management of these patients remains controversial. We reviewed our experience using endoscopic port surgery to identify characteristics that may predict acceptable outcomes., Materials and Methods: We completed a retrospective chart and imaging review of patients who underwent endoscopic port surgery for evacuation of spontaneous ICH at a single center. Data were gathered regarding patient demographics, hemorrhage locations, operative findings, and clinical outcomes., Results: From 2007 to 2011, 18 patients underwent evacuation of spontaneous intracerebral hematomas using an endoscopic port. The mean age in years was 62 years (range, 43-84 years). Six of 18 patients (33%) died before discharge, and 2 others (11%) died after at least 1 month of survival. Of 12 initial survivors, all were discharged to a rehabilitation or nursing facility. Complete hematoma evacuation was achieved in 7 of 18 patients, with the remaining 11 having a partial evacuation. The patients who died (n = 6) before discharge were statistically more likely to have a left-sided hemorrhage, partial evacuation, or older age than the survivors; death at least 1  month after evacuation was additionally associated with greater preoperative hematoma volumes., Conclusions: Our series demonstrates that endoscopic port surgery for acute intracerebral hematoma evacuation has the ability to achieve significant decompression of large and deep-seated hematomas. Patient age, extent of evacuation, laterality, and preoperative hematoma volume appear to influence patient outcome. Most overall outcomes remain poor. Future studies are necessary to determine if surgical evacuation is in fact superior to best medical treatment and if so, to validate, refute, or further identify characteristics that define surgical candidates., (Georg Thieme Verlag KG Stuttgart · New York.)

Background: Intraventricular lesions are challenging entities that may be difficult to resect completely and safely, especially larger lesions with high vascularity or firm consistency., Objective: To assess the results of stereotactically guided endoscopic port (SEP) surgery for resection of colloid cysts and intraventricular tumors., Methods: The authors developed a minimally invasive microsurgical technique for intraventricular surgery using parallel endoscopy to visualize the lesion. Surgical resection was performed via an 11.5-mm transparent conduit (Neuroendoport) deployed under stereotactic guidance. Forty-seven consecutive cases were performed, and all had a minimum 1-year follow-up to assess the efficacy of the technique., Results: For colloid cysts, gross total resection was achieved in 31 (96.9%) of the 32 cases. The transient neurologic morbidity rate was 9.4%; no permanent neurologic morbidity occurred. For intraventricular tumors, gross or near total resection was achieved in 80% of cases. The transient neurological morbidity rate was 6.7%, and no permanent neurological morbidity occurred., Conclusion: SEP surgery for colloid cysts and intraventricular tumors proved to be a safe and effective alternative to conventional microsurgical resection. This technique was not limited by the vascularity, friability, or size of any of the lesions.

The tyrosine phosphorylation sites of the Disabled 1 (Dab1) docking protein are essential for the transmission of the Reelin signal, which regulates neuronal placement. Here we identify Nck beta as a phosphorylation-dependent, Dab1-interacting protein. The SH2 domain of Nck beta but not Nck alpha binds Dab1 phosphorylated on the Reelin-regulated site, Y220, or on Y232. Nck beta is coexpressed with Dab1 in the developing brain and in cultured neurons, where Reelin stimulation leads to the redistribution of Nck beta from the cell soma into neuronal processes. We found that tyrosine-phosphorylated Dab1 in synergy with Nck beta disrupts the actin cytoskeleton in transfected cells. In Drosophila melanogaster, exogenous expression of mouse Dab1 causes tyrosine phosphorylation site-dependent morphological changes in the compound eye. This phenotype is enhanced by overexpression of the Drosophila Nck protein Dock, suggesting a conserved interaction between the Disabled and Nck family members. We suggest a model in which Dab1 phosphorylation leads to the recruitment of Nck beta to the membrane, where it acts to remodel the actin cytoskeleton.