World Neurosurg
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The association between SLC10A3 (solute carrier family 10 member 3) and lower grade glioma (LGG) remains unclear. ⋯ SLC10A3 is a potential diagnostic and prognostic biomarker for LGG and might be associated with substance transport, neurogenic signaling, immune infiltration, and programmed cell death in LGG.
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Neuroendoscopic procedures inside the ventricular system always bear the risk for an unexpected intraoperative hemorrhage. Most hemorrhages can be managed by constant irrigation with low- and high-pressure washes. ⋯ Postoperative magnetic resonance imaging showed complete removal of the left frontal tumor infiltration at the level of the left frontal ependyma. The small residual tumor on the left frontal horn was removed using microsurgical technique with another procedure and after achieving complete removal of all visible tumor, the patient was referred to radiotherapy.
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Orbital cavernous hemangiomas are the most common adult benign vascular orbital neoformation, representing 5%-15% of all orbital masses, and may involve the extraconal or intraconal space.1 According to the International Society for the Study of Vascular Anomalies, orbital cavernous hemangiomas should be classified as low-flow nondistensible venous malformations and are characterized by slow growth, generally 0.2 cm3/year.2,3 For these characteristics, complete surgical resection is necessary for symptomatic patients or in case of significant volumetric increase in its size.4Video 1 demonstrates the cryo-assisted removal of an intraconal orbital hemangioma (22 × 26 mm) located in the superior-lateral aspect of the right orbit in a 55-year-old woman. The patient presented with right exophthalmos and diplopia on right lateral gaze. The lesion was completely removed using a right lateral orbitotomy combined with a superior eyelid endoscopic-assisted approach. ⋯ Exophthalmos resolved postoperatively, without any cosmetic sequelae or visual impairment. Magnetic resonance imaging performed 8 months after surgery demonstrated excellent surgical outcomes, with complete resolution of the exophthalmos and without evidence of persistence of disease. A multidisciplinary approach, involving different specialists familiar with orbital anatomy and physiology, is fundamental in the management of these rare orbital pathologies.
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Facial nerve hemangiomas are a rare entity of skull base lesions that arise within the temporal bone and affect the seventh cranial nerve.1 They are vascular malformations arising from the vascular plexuses surrounding the nerve. Although slow growing and overall benign in nature, they can cause significant facial nerve dysfunction even at small sizes.2 Facial nerve hemangiomas can arise within different segments of the facial nerve within the temporal bone, but most commonly arise near the geniculate ganglion.3 We describe the case of a 34-year-old female who presented with progressive right facial palsy (House-Brackmann 4) and a calcified lesion arising from the petrous temporal bone. Resection of the lesion was performed with a posterior to anterior middle fossa approach, with identification of the greater superficial petrosal nerve and geniculate ganglion, sectioning of the middle meningeal artery, and identification of V2 and V3 segments of the trigeminal nerve (Video 1). ⋯ Postoperative imaging showed gross total resection, and the patient's facial palsy improved to House-Brackmann 1. A comprehensive literature review on surgical approaches and outcomes for the resection of hemangiomas involving the geniculate ganglion or the facial nerve is also provided.2,4-18 The case presentation, surgical anatomy, operative nuances with technical considerations, and postoperative course with imaging are reviewed. The patient and family provided informed consent for the procedure and publication of patient images.
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Acute subdural hematoma (ASDH) leads to the highest mortality rates of all head injuries with secondary brain damage playing a pivotal role in terms of morbidity and mortality. In patients with ASDH, a delay in surgery leads to disproportional mortality. The benefit of (very) early therapy is therefore, a target of ongoing research. As the process of delayed brain damage in ASDH has not yet been described, this study therefore aimed to examine secondary lesion growth in an experimental rat model of ASDH to define the ideal timing for testing potential neuroprotective therapies. ⋯ The most damage develops between 15 minutes and 1 hour and again between 2 and 6 hours after ASDH. The time course of lesion growth supports the approach of early surgery for patients. It furthermore constitutes a basis for further ASDH research with more clearly defined time windows for therapy in animal models.