Spinal Cord Compression Secondary to Metastatic Sinonasal Undifferentiated Carcinoma

Sinonasal undifferentiated carcinoma (SNUC) is a rare malignancy of the upper airways and anterior skull base that carries a poor prognosis. The tumor is known to be invasive into the surrounding structures of the skull base and brain. To date, there is only one existing case report documenting drop metastasis to the intradural extramedullary spinal cord. To the best of our knowledge, we present the second case of metastatic SNUC to the spine. This report describes a 59-year-old male with a history of head and neck SNUC who presented with thoracic back pain and bilateral lower extremity paresis. Neuroimaging demonstrated an extradural thoracic mass with severe spinal cord compression. The patient underwent thoracic laminectomy and fusion for decompression of the spinal cord and internal stabilization. The pathology returned as SNUC. The patient was subsequently lost to follow-up from our institution. Metastatic SNUC is rare. We discuss the relevant clinical imaging and review the literature. Such a malignancy portends a very poor prognosis

Does Combined Therapy of Curcumin and Epigallocatechin Gallate have a synergistic Neuroprotective Effect Aainst Spinal Cord Injury?

Systematic inflammatory response after spinal cord injury (SCI) is one of the factors leading to lesion development and a profound degree of functional loss. Anti-inflammatory compounds, such as curcumin and epigallocatechin gallate (EGCG) are known for their neuroprotective effects. In this study, we investigated the effect of combined therapy of curcumin and EGCG in a rat model of acute SCI induced by balloon compression. Immediately after SCI, rats received curcumin, EGCG, curcumin + EGCG or saline [daily intraperitoneal doses (curcumin, 6 mg/kg; EGCG 17 mg/kg)] and weekly intramuscular doses (curcumin, 60 mg/kg; EGCG 17 mg/kg)] for 28 days. Rats were evaluated using behavioral tests (the Basso, Beattie, and Bresnahan (BBB) open-field locomotor test, flat beam test). Spinal cord tissue was analyzed using histological methods (Luxol Blue-cresyl violet staining) and immunohistochemistry (anti-glial fibrillary acidic protein, anti-growth associated protein 43). Cytokine levels (interleukin-1beta, interleukin-4, interleukin-2, interleukin-6, macrophage inflammatory protein 1-alpha, and RANTES) were measured using Luminex assay. Quantitative polymerase chain reaction was performed to determine the relative expression of genes (Sort1, Fgf2, Irf5, Mrc1, Olig2, Casp3, Gap43, Gfap, Vegf, NfkappaB, Cntf) related to regenerative processes in injured spinal cord. We found that all treatments displayed significant behavioral recovery, with no obvious synergistic effect after combined therapy of curcumin and ECGC. Curcumin and EGCG alone or in combination increased axonal sprouting, decreased glial scar formation, and altered the levels of macrophage inflammatory protein 1-alpha, interleukin-1beta, interleukin-4 and interleukin-6 cytokines. These results imply that although the expected synergistic response of this combined therapy was less obvious, aspects of tissue regeneration and immune responses in severe SCI were evident

Robust estimation of bacterial cell count from optical density

Optical density (OD) is widely used to estimate the density of cells in liquid culture, but cannot be compared between instruments without a standardized calibration protocol and is challenging to relate to actual cell count. We address this with an interlaboratory study comparing three simple, low-cost, and highly accessible OD calibration protocols across 244 laboratories, applied to eight strains of constitutive GFP-expressing E. coli. Based on our results, we recommend calibrating OD to estimated cell count using serial dilution of silica microspheres, which produces highly precise calibration (95.5% of residuals <1.2-fold), is easily assessed for quality control, also assesses instrument effective linear range, and can be combined with fluorescence calibration to obtain units of Molecules of Equivalent Fluorescein (MEFL) per cell, allowing direct comparison and data fusion with flow cytometry measurements: in our study, fluorescence per cell measurements showed only a 1.07-fold mean difference between plate reader and flow cytometry data

Development of a Delayed Posttraumatic Acute Subdural Hematoma

BACKGROUND: Prior studies have shown that most patients with mild traumatic brain injury (TBI) or negative computed tomography (CT) scans of the head rarely decline or require neurosurgical interventions. One common reason for a delayed decline is an intracranial hemorrhage which presents within 24 to 48 hours. This is typically seen in elderly patients and/or patients on antiplatelet or anticoagulation agents. We describe a case of a delayed subdural hemorrhage presenting in a young adult not on any antiplatelet or anticoagulation therapy. CASE DESCRIPTION: A 19 year old male presented to the emergency room after being involved in a motor vehicle accident. He had a Glasgow coma scale of 15 and an initial CT was negative for any intracranial hemorrhage or pathology, so he was then admitted to the ICU for further care. The patient received one dose of aspirin 325mg the following day for treatment of blunt cerebrovascular injury. 6 hours later he reported a severe headache and had an episode of emesis with a subsequent rapid neurologic decline. A repeat CT showed an acute right subdural hematoma and he underwent an emergent right decompressive hemicraniectomy. CONCLUSION: In rare cases, patients with negative initial head CT scans neurologically deteriorate as a result of a delayed acute subdural hematoma. We present an unusual case of a young patient on no medications with no CT findings of an intracranial injury who neurologically declined due to a delayed acute subdural hematoma

Spontaneous Spinal Epidural Hematoma in an Infant

A spontaneous spinal epidural hematoma is a collection of blood in the spinal epidural space that occurs in the absence of trauma. They most commonly present in the fourth to fifth decade in life with acute onset neck or back pain with delayed neurologic deficit. However, this presentation is often complicated in children because of the limitations in the pediatric neurologic exam. Magnetic resonance imaging is the imaging modality of choice for diagnosis. Here is a rare case of an infant spontaneous spinal epidural hematoma whose diagnosis was delayed because of a recent history of fever and viral pharyngitis before his development of neurologic deficits. Spontaneous spinal epidural hematomas are a rare phenomenon, which often present with nonspecific symptoms in the pediatric population. This diagnosis should be considered to initiate treatment in a timely manner. The treatment typically is emergent surgical decompression to minimize the risk of permanent neurologic deficit

Retrosigmoid Craniectomy for Resection of Epidermoid causing Trigeminal Neuralgia

The differential diagnosis for trigeminal neuralgia like-symptoms includes cerebellopontine angle lesions causing regional mass effect upon the trigeminal nerve ( Fig. 1 ). Here we present an operative video manuscript of a patient experiencing trigeminal neuralgia, secondary to an epidermoid cyst, in which a retrosigmoid craniectomy was performed to resect the epidermoid and decompress the trigeminal nerve ( Fig. 2 ). This video highlights the operative nuances to achieving a successful surgery, including appropriate patient positioning, dural exposure to the transverse-sigmoid sinus junction, arachnoid dissection, and decompression of cranial nerves. A gross total resection was achieved; the patient reported immediate relief of facial pain postoperatively and has been pain free at the ten month follow-up. The link to the video can be found at: https://youtu.be/Ja2eE0uGk4E

Targeting the mTOR Pathway Using Novel ATP‑Competitive Inhibitors, Torin1, Torin2 and XL388, in the Treatment of Glioblastoma

Mechanistic target of rapamycin (mTOR), which functions via two multiprotein complexes termed mTORC1 and mTORC2, is positioned in the canonical phosphoinositide 3‑kinase‑related kinase (PI3K)/AKT (PI3K/AKT) pathways. These complexes exert their actions by regulating other important kinases, such as 40S ribosomal S6 kinases (S6K), eukaryotic translation initiation factor 4E (elF4E)‑binding protein 1 (4E‑BP1) and AKT, to control cell growth, proliferation, migration and survival in response to nutrients and growth factors. Glioblastoma (GB) is a devastating form of brain cancer, where the mTOR pathway is deregulated due to frequent upregulation of the Receptor Tyrosine Kinase/PI3K pathways and loss of the tumor suppressor phosphatase and tensin homologue (PTEN). Rapamycin and its analogs were less successful in clinical trials for patients with GB due to their incomplete inhibition of mTORC1 and the activation of mitogenic pathways via negative feedback loops. Here, the effects of selective ATP‑competitive dual inhibitors of mTORC1 and mTORC2, Torin1, Torin2 and XL388, are reported. Torin2 exhibited concentration‑dependent pharmacodynamic effects on inhibition of phosphorylation of the mTORC1 substrates S6KSer235/236 and 4E‑BP1Thr37/46 as well as the mTORC2 substrate AKTSer473 resulting in suppression of tumor cell migration, proliferation and S‑phase entry. Torin1 demonstrated similar effects, but only at higher doses. XL388 suppressed cell proliferation at a higher dose, but failed to inhibit cell migration. Treatment with Torin1 suppressed phosphorylation of proline rich AKT substrate of 40 kDa (PRAS40) at Threonine 246 (PRAS40Thr246) whereas Torin2 completely abolished it. XL388 treatment suppressed the phosphorylation of PRAS40Thr246 only at higher doses. Drug resistance analysis revealed that treatment of GB cells with XL388 rendered partial drug resistance, which was also seen to a lesser extent with rapamycin and Torin1 treatments. However, treatment with Torin2 completely eradicated the tumor cell population. These results strongly suggest that Torin2, compared to Torin1 or XL388, is more effective in suppressing mTORC1 and mTORC2, and therefore in the inhibition of the GB cell proliferation, dissemination and in overcoming resistance to therapy. These findings underscore the significance of Torin2 in the treatment of GB