Retinal ganglion cells (RGCs), the projection neurons of the eye, cannot regenerate their axons once the optic nerve has been injured and soon begin to die. Whereas RGC death and regenerative failure are widely viewed as being cell-autonomous or influenced by various types of glia, we report here that the dysregulation of mobile zinc (Zn 2+ ) in retinal interneurons is a primary factor. Within an hour after the optic nerve is injured, Zn 2+ increases several-fold in retinal amacrine cell processes and continues to rise over the first day, then transfers slowly to RGCs via vesicular release. Zn 2+ accumulation in amacrine cell processes involves the Zn 2+ transporter protein ZnT-3, and deletion of slc30a3, the gene encoding ZnT-3, promotes RGC survival and axon regeneration. Intravitreal injection of Zn 2+ chelators enables many RGCs to survive for months after nerve injury and regenerate axons, and enhances the prosurvival and regenerative effects of deleting the gene for phosphatase and tensin homolog (pten). Importantly, the therapeutic window for Zn 2+ chelation extends for several days after nerve injury. These results show that retinal Zn 2+ dysregulation is a major factor limiting the survival and regenerative capacity of injured RGCs, and point to Zn 2+ chelation as a strategy to promote long-term RGC protection and enhance axon regeneration.T he optic nerve has been widely used to investigate the response of CNS neurons to injury because of its accessibility, anatomy, and functional importance. Under normal circumstances, retinal ganglion cells (RGCs), the projection neurons of the eye, cannot regenerate axons after the optic nerve has been damaged and soon undergo cell death, leaving victims of traumatic or ischemic nerve injury or degenerative conditions, such as glaucoma, with permanent visual losses. Optic nerve injury leads to numerous pathological changes in RGCs and reversing some of these changes improves cell survival, although these effects are often transitory and for the most part promote little or no axon regeneration (1-10). Regeneration per se can be induced by intraocular inflammation combined with elevated cAMP (11, 12), counteracting cell-intrinsic (13-15) or cellextrinsic (16, 17) suppressors of axon growth, oncomodulin and other growth factors (18-22), or elevated physiological activity (23,24). Some of these treatments act synergistically and enable a modest number of RGCs to reestablish connections with appropriate target areas in the brain (25-27). However, although these studies show that successful regeneration can occur in principle, most RGCs eventually die after optic nerve injury, and to date only a small fraction of surviving RGCs have been induced to regenerate axons (27). These observations imply the existence of other major, as yet unknown suppressors of cell survival and regeneration. Our results point to zinc dysregulation as a critical factor.Zinc is essential for many cellular functions. Covalently bound zinc is required for the activity of numerous enzymes and t...

Limiting the spread of the disease is key to controlling the COVID-19 pandemic. This includes identifying people who have been exposed to COVID-19, minimizing patient contact, and enforcing strict hygiene measures. To prevent healthcare systems from becoming overburdened, elective and non-urgent medical procedures and treatments have been postponed, and primary health care has broadened to include virtual appointments via telemedicine. Although telemedicine precludes the physical examination of a patient, it allows collection of a range of information prior to a patient's admission, and may therefore be used in preoperative assessment. This new tool can be used to evaluate the severity and progression of the main disease, other comorbidities, and the urgency of the surgical treatment as well as preferencing anesthetic procedures. It can also be used for effective screening and triaging of patients with suspected or established COVID-19, thereby protecting other patients, clinicians and communities alike.

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Object. The etiology of chronic subdural hematoma (CSDH) in nongeriatric patients (≤ 60 years old) often remains unclear. The primary objective of this study was to identify spinal CSF leaks in young patients, after formulating the hypothesis that spinal CSF leaks are causally related to CSDH.Methods. All consecutive patients 60 years of age or younger who underwent operations for CSDH between September 2009 and April 2011 at Bern University Hospital were included in this prospective cohort study. The patient workup included an extended search for a spinal CSF leak using a systematic algorithm: MRI of the spinal axis with or without intrathecal contrast application, myelography/fluoroscopy, and postmyelography CT. Spinal pathologies were classified according to direct proof of CSF outflow from the intrathecal to the extrathecal space, presence of extrathecal fluid accumulation, presence of spinal meningeal cysts, or no pathological findings. The primary outcome was proof of a CSF leak.Results. Twenty-seven patients, with a mean age of 49.6 ± 9.2 years, underwent operations for CSDH. Hematomas were unilateral in 20 patients and bilateral in 7 patients. In 7 (25.9%) of 27 patients, spinal CSF leakage was proven, in 9 patients (33.3%) spinal meningeal cysts in the cervicothoracic region were found, and 3 patients (11.1%) had spinal cysts in the sacral region. The remaining 8 patients (29.6%) showed no pathological findings.Conclusions. The direct proof of spinal CSF leakage in 25.9% of patients suggests that spinal CSF leaks may be a frequent cause of nongeriatric CSDH. (http://thejns.org/doi/abs/10.3171/2014.6.JNS14550) key WorDS • chronic subdural hematoma • spinal CSF leak • geriatric • vascular disorders • meningeal cyst Abbreviations used in this paper: CSDH = chronic subdural hematoma; mRS = modified Rankin Scale; SIH = spontaneous intracranial hypotension; SPACE = sampling perfection with application of optimized contrasts using different flip angle evolutions.

Using 5-aminolevulinic acid imaging and intraoperative mapping/monitoring together leads to a high rate of CRET and an increased rate of GTR compared with the literature without increasing the rate of permanent morbidity. The combination of safety and resection-enhancing intraoperative technologies was likely to be the major drivers for this high rate of CRET/GTR.

Cranioplasty is a common neurosurgical procedure. Free-hand molding of polymethyl methacrylate (PMMA) cement into complex three-dimensional shapes is often time-consuming and may result in disappointing cosmetic outcomes. Computer-assisted patient-specific implants address these disadvantages but are associated with long production times and high costs. In this study, we evaluated the clinical, radiological, and cosmetic outcomes of a timesaving and inexpensive intraoperative method to mold custom-made implants for immediate single-stage or delayed cranioplasty. Data were collected from patients in whom cranioplasty became necessary after removal of bone flaps affected by intracranial infection, tumor invasion, or trauma. A PMMA replica was cast between a negative form of the patient's own bone flap and the original bone flap with exactly the same shape, thickness, and dimensions. Clinical and radiological follow-up was performed 2 months post-surgery. Patient satisfaction (Odom criteria) and cosmesis (visual analogue scale for cosmesis) were evaluated 1 to 3 years after cranioplasty. Twenty-seven patients underwent intraoperative template-molded patient-specific cranioplasty with PMMA. The indications for cranioplasty included bone flap infection (56%, n015), calvarian tumor resection (37%, n010), and defect after trauma (7%, n02). The mean duration of the molding procedure was 19±7 min. Excellent radiological implant alignment was achieved in 94% of the cases. All (n023) but one patient rated the cosmetic outcome (mean 1.4 years after cranioplasty) as excellent (70%, n016) or good (26%, n06). Intraoperative cast-molded reconstructive cranioplasty is a feasible, accurate, fast, and cost-efficient technique that results in excellent cosmetic outcomes, even with large and complex skull defects.Keywords Patient-specific implant . Cranioplasty . Skull bone flap . Bone replacement material polymethyl methacrylate-PMMA . Brain tumors . Trauma . Brain

While dopamine-agonists are the first-line approach in treating prolactinomas, surgery can be considered in selected cases besides non-responders or patients with dopamine-agonist intolerance. The aim of the present study was to compare the long-term outcome in women with prolactinomas treated primarily either surgically or medically who had not had prior dopamine-agonist treatment. Retrospective case-note study of all consecutive women with prolactinomas primarily managed with medical therapy or surgery in a tertiary referral centre. The clinical, biochemical, and radiological responses to first-line treatment at early and long-term follow-up were analysed. The primary therapeutic strategy was dopamine-agonists for 36 (34 %) and surgery for 71 (66 %) of the women. Baseline clinical and biochemical characteristics were not significantly different between the primary surgical and medical cohort. Median follow-up time was 90 months (range 13-408). Following primary treatment, prolactin level significantly decreased in both cohorts, on average to 13.5 µg/L (IQR 7-21; p < 0.001), and was within the normal range in 82 % of all patients. No women in the surgical cohort demonstrated permanent sequelae and morbidity was low. At final follow-up, control of hyperprolactinaemia required dopamine-agonist therapy in 64 % of women who had undergone primary medical therapy vs. 32 % of those who had primary surgical therapy (p = 0.003). Logistic regression revealed that the primary therapeutic strategy, but not adenoma size, was an independent risk factor for long-term dependence on dopamine-agonists. The present data indicate that in a dedicated tertiary referral centre, long-term control of hyperprolactinaemia in women with prolactinomas is high. In selected cases, a primary neurosurgical approach might at least be interdisciplinarily discussed with the primary goal of minimizing long-term dependence on dopamine-agonists.

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