A rare encounter: Comprehensive case review of myxoid meningiomas with a representative case.

Meningiomas are the most diagnosed primary central nervous system tumor. Currently, 15 different subtypes of meningioma exist with various characteristics. One extremely rare subtype is myxoid meningioma, which is a World Health Organization grade 1 benign meningioma. These specific meningiomas have only been reported 12 times in the literature. In this representative case, we present a 46-year-old female patient with a left frontal myxoid meningioma, describe the findings on imaging, and provide the histopathological features that are needed for diagnosis. Furthermore, this report discusses the other existing myxoid meningioma case reports found throughout the literature.

PRMT7 can prevent neurovascular uncoupling, blood-brain barrier permeability, and mitochondrial dysfunction in repetitive and mild traumatic brain injury.

Mild traumatic brain injury (TBI) comprises the largest percentage of TBI-related injuries, with pathophysiological and functional deficits that persist in a subset of TBI patients. In our three-hit paradigm of repetitive and mild traumatic brain injury (rmTBI), we observed neurovascular uncoupling via decreased red blood cell velocity, microvessel diameter, and leukocyte rolling velocity 3 days post-rmTBI via intra-vital two-photon laser scanning microscopy. Furthermore, our data suggest increased blood-brain barrier (BBB) permeability (leakage), with corresponding decrease in junctional protein expression post-rmTBI. Mitochondrial oxygen consumption rates (measured via Seahorse XFe24) were also altered 3 days post-rmTBI, along with disrupted mitochondrial dynamics of fission and fusion. Overall, these pathophysiological findings correlated with decreased protein arginine methyltransferase 7 (PRMT7) protein levels and activity post-rmTBI. Here, we increased PRMT7 levels in vivo to assess the role of the neurovasculature and mitochondria post-rmTBI. In vivo overexpression of PRMT7 using a neuronal specific AAV vector led to restoration of neurovascular coupling, prevented BBB leakage, and promoted mitochondrial respiration, altogether to suggest a protective and functional role of PRMT7 in rmTBI.

A role for protein arginine methyltransferase 7 in repetitive and mild traumatic brain injury.

Mild traumatic brain injury affects the largest proportion of individuals in the United States and world-wide. Pre-clinical studies of repetitive and mild traumatic brain injury (rmTBI) have been limited in their ability to recapitulate human pathology (i.e. diffuse rotational injury). We used the closed-head impact model of engineered rotation acceleration (CHIMERA) to simulate rotational injury observed in patients and to study the pathological outcomes post-rmTBI using C57BL/6J mice. Enhanced cytokine production was observed in both the cortex and hippocampus to suggest neuroinflammation. Furthermore, microglia were assessed via enhanced iba1 protein levels and morphological changes using immunofluorescence. In addition, LC/MS analyses revealed excess glutamate production, as well as diffuse axonal injury via Bielschowsky's silver stain kit. Moreover, the heterogeneous nature of rmTBI has made it challenging to identify drug therapies that address rmTBI, therefore we sought to identify novel targets in the concurrent rmTBI pathology. The pathophysiological findings correlated with a time-dependent decrease in protein arginine methyltransferase 7 (PRMT7) protein expression and activity post-rmTBI along with dysregulation of PRMT upstream mediators s-adenosylmethionine and methionine adenosyltransferase 2 (MAT2) in vivo. In addition, inhibition of the upstream mediator MAT2A using the HT22 hippocampal neuronal cell line suggest a mechanistic role for PRMT7 via MAT2A in vitro. Collectively, we have identified PRMT7 as a novel target in rmTBI pathology in vivo and a mechanistic link between PRMT7 and upstream mediator MAT2A in vitro.

The Management of Recurrent Post-myelography Lumbar Pseudomeningocele With Epidural Blood Patch.

Pseudomeningoceles are a well-known potential postoperative complication of spinal and cranial surgeries that can occur after lumbar decompression and posterior fossa surgeries. They are often caused by incidental durotomies but may also occur as a result of dural puncture during diagnostic testing. This report describes a 59-year-old male that developed a recurrent pseudomeningocele after an L4 laminectomy for severe lumbar spinal stenosis that was ultimately treated with an epidural blood patch (EBP). His preoperative condition greatly improved, but he developed a pseudomeningocele that did not resolve after applying ice and light pressure. The patient subsequently underwent a wound exploration where no dural defect was identified. During this exploration, the dura was reinforced with dural onlays and sealant. Unfortunately, the patient developed another pseudomeningocele within a short interval. It was then suspected that the post-laminectomy site provided a space for the dural punctures from previous CT myelography to leak cerebrospinal fluid (CSF) into. The patient subsequently underwent ultrasound (US)-guided aspiration of the pseudomeningocele and EBP injections at the levels where his preoperative myelography was performed. The success of the EBP indicates that the previous CT myelography was the likely cause of the pseudomeningocele. Recurrent spinal pseudomeningoceles with no evidence of incidental durotomy may be caused by dural puncture from myelography. In such cases, EBP to the area that the previous myelography was performed can resolve the pseudomeningocele.

Neurologic Complications in Patients with Left Ventricular Assist Devices: Single Institution Retrospective Review.

BACKGROUND: Neurologic complications are common complications encountered by patients with left ventricular assist devices (LVADs). This single-center retrospective study aims to identify the incidence and risk factors of neurologic complications and interventions in patients supported with LVADs and define the associated anticoagulation management. METHODS: Between August 2009 and August 2017, 244 patients underwent LVAD implantation. Twenty-one patients were excluded for having neurologic complications before LVAD placement or for having previously undergone heart transplantation. RESULTS: Fifty-six patients (25%) suffered 61 complications, and 11 (19.6%) died as a result. Gender, type of LVAD, or chronic medical comorbidities evaluated did not contribute to a difference in complication rate; in contrast, length of LVAD implantation was directly related to risk of neurologic complication. Eleven patients (19.6%) underwent 13 surgical interventions including 5 mechanical thrombectomies. Anticoagulation was reversed in 16 patients and held without complication. Anticoagulation was not held for ischemic complications, and no clinically significant hemorrhagic transformation occurred. Intravenous tissue plasminogen activator was also successfully administered to 3 patients without complication. CONCLUSIONS: Neurologic complications were observed in 25% of patients supported with LVADs, of which 20% required neurosurgical intervention. Anticoagulation can be safely withheld in patients with hemorrhagic complications. Patients with ischemic complications can continue to be anticoagulated with no significant risk of hemorrhagic transformation. Length of LVAD implantation was directly related to the risk of neurologic complication. Finally, our study adds to existing literature that mechanical thrombectomy and even intravenous tissue plasminogen activator are options for LVAD patients with ischemic complications.