Rejected

In December 2019, in Wuhan, a new virus emerged, causing severe acute respiratory syndrome (SARS) secondary to infection by a type of coronavirus, causing coronavirus disease (COVID-19). The pandemic caused by the new coronavirus has had implications in the central nervous system. COVID-19 is known to be characterized by coagulation activation and endothelial dysfunction, causing ischemic and hemorrhagic vascular syndromes.

: Many pieces of research have focused on pain within individuals, but little attention has been paid to whether pain can change an individual's empathic ability and affect social relationships. The purpose of this study is to explore how chronic low back pain changes empathy. : Twenty-four chronic low back pain patients and 22 healthy controls were recruited. We set up an experimental pain-exposed model for each healthy subject. All subjects received a painful-empathic magnetic resonance scan. After the scan, all subjects rated the pain intensity and multiple empathy-related indicators. The clinical assessment scale was the 20-item Basic Empathy Scale in Adults. : The chronic low back pain patients reported lower scores on the total scores of BES-A, the subscale scores of emotional disconnection and cognitive empathy, and the discomfort rating. The fMRI results in the chronic low back pain patients showed that there were multiple abnormal brain pathways centered on the anterior insula. The DTI results in the chronic low back pain patients showed that there were reduced fractional anisotropy values in the corpus callosum, bilateral anterior thalamic radiation (ATR), right posterior thalamic radiation (PTR), right superior longitudinal fasciculus (SLF), and left anterior corona radiate (ACR). : Our study found that patients with chronic low back pain have impaired empathy ability. The abnormal functional connectivity of multiple brain networks, multiple damaged white matter tracts, and the lower behavioral scores in chronic low back pain patients supported our findings.

COVID-19 is a pandemic disease and questions rise about the coronavirus 2 (Sars-CoV-2) effect on nervous system. This involvement could help explaining the pathogenesis of this condition and lead to novel therapeutic approaches.

Salmonella is an extremely rare cause of an infected endometrioma. We present a case of a 30-year-old immunocompetent woman presenting with fevers and abdominal pain, on a background of prior endometriosis. Initial antibiotic treatment for pelvic inflammatory disease failed, and the patient progressed to septic shock requiring surgical evacuation of an infected ovarian endometrioma. Microbiological samples from stool, ovary, and peritoneal fluid revealed infection with . The likely diagnosis was Salmonella enterocolitis with bacterial translocation to an ovarian endometrioma.

Modern head-mounted displays (HMDs) are a promising technology. Thanks to their affordable cost and versatility, HMDs are gaining attention from different sectors. However, the experience reported by the users of these technologies is sometimes negative. A number of people, when using an HMD, complain of various types of physical discomfort as well as symptoms like headache, disorientation, and nausea. These symptoms, developed during or after exposure to virtual environments, are commonly referred to with the term simulator sickness. Some scientific studies have shown that women are commonly more sensitive to simulator sickness. However, a gender imbalance in the susceptibility to simulator sickness has not been widely studied in the context of modern HMDs, and the studies that have been done have reported heterogeneous findings. The present systematic review aims to gather the pieces of evidence that support and oppose a gender difference in the susceptibility of simulator sickness in the framework of modern HMDs. We also aim to individuate other gender differences in the experience of the use of these technologies to establish whether there is sufficient evidence to support a gender discrepancy in the user experience.

T-cell large granular lymphocytic leukemia is characterized by clonal expansion of a CD3/CD57 subpopulation, which are typically CD8 positive cytotoxic T- cells, and can only be diagnosed if there is a persistent, greater than 6 months, elevation of LGL in the blood (usually 2-20 × 10/L), in the absence of an identifiable cause. T-LGLL has been associated with reactive conditions such as autoimmune diseases and viral infections and has also been reported in association with hematologic and non-hematologic malignancies. We report a case of asymptomatic CD4/CD8 double-positive T-LGLL. Flow cytometry on peripheral blood revealed a subpopulation of CD4/CD8 double-positive T cells expressing CD57 and cTIA. Clonality was established by flow cytometric analysis of T-cell receptor () region repertoire which showed that >70% of the cells failed to express any of the tested () regions. Clonality was further confirmed by PCR with the detection of clonal TCR beta and TCR gamma gene rearrangements. Six months later, she presented with persistent lower back pain and diagnosed with IgG kappa multiple myeloma. CD4/CD8 double-positive T-large granular leukemia is the first case reported in the literature. This rare phenotype is either underreported or a truly rare clinical entity. More studies are warranted to characterize the pathogenesis and clinical characteristics of this group of patients and to further assess the relationship between multiple myeloma and T-LGLL as a cause-and-effect relationship or simply related to the time at which diagnosis has been made.

Poor postoperative pain (POP) control increases perioperative morbidity, prolongs hospitalization days, and causes chronic pain. However, the specific mechanism(s) underlying POP is unclear and the identification of optimal perioperative treatment remains elusive. Akt and mammalian target of rapamycin (mTOR) are expressed in the spinal cord, dorsal root ganglion, and sensory axons. In this study, we explored the role of Akt and mTOR in pain-related behaviors induced by plantar incision in mice. Plantar incision activated spinal Akt and mTOR in a dose-dependent manner. Pre-treatment with Akt inhibitors intrathecally prevented the activation of mTOR dose-dependently. In addition, blocking the Akt-mTOR signaling cascade attenuated pain-related behaviors and spinal Fos protein expression induced by plantar incision. Our observations demonstrate that Akt-mTOR might be a potential therapeutic target for the treatment of POP.

As neurologists earn their living with the preservation and restoration of brain function, they are also well-positioned to address the science behind the transition from life to death. This essay in pictures highlights areas of neurological expertise needed for brain death determination; shows pitfalls to avoid during the clinical examination and interpretation of confirmatory laboratory tests in brain death protocols; illustrates the great variability of brain death legislations around the world; discusses arguments for the implementation of donation after circulatory death (DCD); points to unresolved questions related to DCD and the time between cardiac standstill and organ procurement ("hands-off period"); provides an overview of the epidemiology and semiology of near-death experiences, including their importance for religion, literature, and the visual arts; suggests biological mechanisms for near-death experiences such as dysfunction of temporoparietal cortex, N-methyl-D-aspartate receptor antagonism, migraine aura, and rapid eye movement sleep; hypothesizes that thanatosis (aka. death-feigning, a common behavioral trait in the animal kingdom) represents the evolutionary origin of near-death experiences; and speculates about the future implications of recent attempts of brain resuscitation in an animal model. The aim is to provide the reader with a thorough understanding that the boundaries within the neurology of death and the dying brain are being pushed just like everywhere else in the clinical neurosciences.

We investigated whether chronic sciatic ligation modifies the glutamate release in spinal cord nerve endings (synaptosomes) as well as the expression and the function of presynaptic release-regulating mGlu2/3 autoreceptors and 5-HT heteroreceptors in these particles. Synaptosomes were from the spinal cord of animals suffering from the sciatic ligation that developed on day 6 post-surgery a significant decrease of the force inducing paw-withdrawal in the lesioned paw. The exocytosis of glutamate (quantified as release of preloaded [H]D-aspartate, [H]D-Asp) elicited by a mild depolarizing stimulus (15 mM KCl) was significantly increased in synaptosomes from injured rats when compared to controls (uninjured rats). The mGlu2/3 agonist LY379268 (1000 pM) significantly inhibited the 15 mM KCl-evoked [H]D-Asp overflow from control synaptosomes, but not in terminals isolated from injured animals. Differently, a low concentration (10 nM) of (±) DOI, unable to modify the 15 mM KCl-evoked [H]D-Asp overflow in control spinal cord synaptosomes, significantly reduced the glutamate exocytosis in nerve endings isolated from the injured rats. Acute oral trazodone (TZD, 0.3 mg/kg on day 7 post-surgery) efficiently recovered glutamate exocytosis as well as the efficiency of LY379268 in inhibiting this event in spinal cord synaptosomes from injured animals. The sciatic ligation significantly reduced the expression of mGlu2/3, but not of 5-HT, receptor proteins in spinal cord synaptosomal lysates. Acute TZD recovered this parameter. Our results support the use of 5-HT antagonists for restoring altered spinal cord glutamate plasticity in rats suffering from sciatic ligation.

Solitary fibrous tumors (SFTs) can occur in several locations outside the pleura, but rarely in the sinonasal tract, and particularly not in the nasopharynx. Herein, we describe an unusual case of giant cell-rich SFT (GCRSFT) occurring in the nasopharynx. A 64-year-old man experienced dizziness and headache for more than 10 years with no obvious cause. Computed tomography (CT) scan showed a 3.9 cm × 2 cm tumor on the posterior lateral wall of the left nasopharynx, and angiography revealed a hypervascular tumor fed by branches of the left carotid artery. Hence, preoperative embolization was performed, and then the tumor was endoscopically resected. The symptoms were relieved after the resection, and postoperative head CT and video laryngoscopy showed that the tumor was completely resected. We next characterized the specific pathological characteristics of the resected tumor. Histologically, the tumor was characterized by varying cellular proliferation of cytologically bland spindle cells within a collagenous stroma, with prominent interspersed branching vessels. Mitotic activity was low (2/50HPF), and there was no evidence of pleomorphism or tumor necrosis. Moreover, multinucleated giant cells with deep nuclear staining and distributed in pseudovascular spaces were found within the tumor. We ruled out the possibility that our case was giant cell fibroblastoma (GCF) by immunohistochemical analysis, showing that the tumor cells were positive for CD34, CD99, STAT6, and BCL-2, and that the Ki-67 labeling index was 3%, indicating that our case was SFT and not GCF. The patient's condition is generally good after a 14-month follow-up. This report serves to broaden the morphologic spectrum of GCRSFT and will help clinicians and pathologists better understand this entity to prevent misdiagnosis.