关键词： melatonin   neurogenesis   neural stem cell   neurogenesis impairment   neurological disorder   molecular mechanism   review  

摘要： Neurogenesis is the process by which functional new neurons are generated from the neural stem cells (NSCs) or neural progenitor cells (NPCs). Increasing lines of evidence show that neurogenesis impairment is involved in different neurological illnesses, including mood disorders, neurogenerative diseases, and central nervous system (CNS) injuries. Since reversing neurogenesis impairment was found to improve neurological outcomes in the pathological conditions, it is speculated that modulating neurogenesis is a potential therapeutic strategy for neurological diseases. Among different modulators of neurogenesis, melatonin is a particularly interesting one. In traditional understanding, melatonin controls the circadian rhythm and sleep-wake cycle, although it is not directly involved in the proliferation and survival of neurons. In the last decade, it was reported that melatonin plays an important role in the regulation of neurogenesis, and thus it may be a potential treatment for neurogenesis-related disorders. The present review aims to summarize and discuss the recent findings regarding the protective effects of melatonin on the neurogenesis impairment in different neurological conditions. We also address the molecular mechanisms involved in the actions of melatonin in neurogenesis modulation.

关键词： consanguineous marriages   homozygous variant   lower limbs weakness   missense variants   NKX6-2 gene   progressive spastic ataxia  

摘要： Background Progressive spastic ataxia is a heterogeneous disorder characterized by cerebellar ataxia and limb spasticity associated with other severe neurological complications. Spastic ataxia is classified into pure and complex types, inherited in both an autosomal recessive and autosomal dominant manner. It is caused by pathogenic variants in at least eight different genes, including NKX6-2 (MIM 607063) located on chromosome 10q26.3. The present study aimed to identify the genetic variant(s) underlying progressive spastic ataxia and to establish the genotype-phenotype correlation. Methods We collected a large consanguineous family having four affected individuals segregating progressive spastic ataxia in an autosomal recessive manner. To investigate the molecular cause of the disease, genomic DNA of three affected individuals underwent whole exome sequencing. Results All of the affected individuals showed progressive clinical features such as spastic ataxia, lower limb weakness and other mild neurological abnormalities. Whole exome sequencing data were analyzed using different filters. Filtering of rare and shared homozygous variants revealed a novel homozygous missense variant (c.545C>T;***182Val) in a highly conserved homeobox domain of the NKX6-2 protein. Conclusions The findings of the present study add a novel variant to the NKX6-2 mutation spectrum and provide evidence that homozygous variants in the NKX6-2 cause progressive spastic ataxia associated with other abnormalities.

关键词： COVID-19   Pandemic   Education   Neurology training  

摘要： Throughout this pandemic, neurology resident education and service has, and will continue to be, affected during this unprecedented time. Balancing the safety of our residents as well as the anticipated inpatient service demands, we have, and continue to, make changes to meet the needs of our community. Education certainly has been affected but we have made great effort to maintain normalcy. We are leveraging web-based technologies to continue formal didactics. The American Academy of Neurology has provided program directors with various tools to share to provide high-yield academic education. AAN Synapse, distance learning modules, and podcasts are a few examples. Each residency training program will likely face different challenges depending on location and community structure. We have an obligation to help all of our colleagues in the hospital in providing quality and compassionate care during this time of need. Our training and education will only benefit from this experience teaching us lessons on adaptability, the importance of teamwork, and self-sacrifice. (C) 2020 Elsevier Ltd. All rights reserved.

关键词： Burst fracture   Thoracolumbar spine   Spinal fracture   Posterior approach   Young patients   Neurological deficits  

摘要： Introduction: Surgical management of thoracolumbar burst fractures is controversial. While the goals of surgical treatment are well accepted (i.e., fracture reduction and stabilization, neural elements decompression, and segmental angular deformity correction), the choice of the best surgical approach (i.e., posterior vs. anterior vs. combined approach) remains controversial. Several studies have debated the advantages of each surgical approach but there is no definitive evidence available to date, particularly in young adult patients. The aim of this study was to assess whether posterior approach alone can be a valid surgical treatment for patient under the age of 40 affected by thoracolumbar burst fractures and incomplete neurological deficits. Material and Methods: A total of 10 consecutive patients affected by thoracolumbar burst fractures associated with incomplete neurological deficits treated at our institution from January 2015 to February 2017 were included in our study. All patients were under the age of 40 at the time of injury and underwent decompression and stabilization using the posterior surgical approach alone. Demographics, clinical, and radiographic parameters were recorded preoperatively, postoperatively and at the latest available follow-up. The minimum follow-up was set at 2 years post-operatively. Results: The mean operative time was 303.6 min (range, 138-486). Average blood loss was 756 mL (range, 440-2100). Nine out of ten patients returned to a normal neurological status after surgery while 1 patient showed some improvement but did not recover completely. Segmental kyphotic deformity improved from a mean of 21.8 degrees before surgery to 14.8 degrees at the time of the last follow-up. The anterior and posterior wall height of the fractured vertebra was restored with an average of 4 mm. The Visual Analogue Scale score reported an improvement from the mean preoperative value of 7.92 to 1.24 at the last follow-up;8 out of 10 patients resumed p

关键词： cerebrovascular diseases   COVID-19   neuro-invasive mechanism   neurological manifestations   SARS-CoV-2  

摘要： Background and purpose Infections with coronaviruses are not always confined to the respiratory tract and various neurological manifestations have been reported. The aim of this study was to perform a review to describe neurological manifestations in patients with COVID-19 and possible neuro-invasive mechanisms of Sars-CoV-2. Methods PubMed, Web of Science and COVID-dedicated databases were searched for the combination of COVID-19 terminology and neurology terminology up to 10 May 2020. Social media channels were followed up between 15 March and 10 May 2020 for postings with the same scope. Neurological manifestations were extracted from the identified papers and combined to provide a useful summary for the neurologist in clinical practice. Results Neurological manifestations potentially related to COVID-19 have been reported in large studies, case series and case reports and include acute cerebrovascular diseases, impaired consciousness, cranial nerve manifestations and autoimmune disorders such as the Guillain-Barre syndrome often present in patients with more severe COVID-19. Cranial nerve symptoms such as olfactory and gustatory dysfunctions are highly prevalent in patients with mild to moderate COVID-19 even without associated nasal symptoms and often present in an early stage of the disease. Conclusion Physicians should be aware of the neurological manifestations in patients with COVID-19, especially when rapid clinical deterioration occurs. The neurological symptoms in COVID-19 patients may be due to direct viral neurological injury or indirect neuroinflammatory and autoimmune mechanisms. No antiviral treatments against the virus or vaccines for its prevention are available and the long-term consequences of the infection on human health remain uncertain especially with regard to the neurological system.

关键词： COVID-19   stroke   symptoms  

关键词： ALS   Huntington's disease   Parkinson's disease   Alzheimer's disease   Ischemia   Seizure   Glutamate   Dopamine   System xc   Cocaine   Alcohol   Opioid  

摘要： Ceftriaxone is a beta-lactam antibiotic that increases the expression of the major glutamate transporter, GLT-1. As such, ceftriaxone ameliorates symptoms across multiple rodent models of neurological diseases and substance use disorders. However, the mechanism behind GLT-1 upregulation is unknown. The present review synthesizes this literature in order to identify commonalities in molecular changes. We find that ceftriaxone (200 mg/kg for at least two days) consistently restores GLT-1 expression in multiple rodent models of neurological disease, especially when GLT-1 is decreased in the disease model. The same dose given to healthy/drug-naive rodents does not reliably upregulate GLT-1 in any brain region except the hippocampus. Increased GLT-1 expression does not consistently arise from transcriptional regulation, and is likely to be due to trafficking changes. In addition to altered transporter expression, ceftriaxone ameliorates neuropathologies (e.g. tau, amyloid beta, cell death) and aberrant protein expression associated with a number of neurological disease models. Taken together, these results indicate that ceftriaxone remains a strong candidate for treatment of multiple disorders in the clinic.

摘要： Dialysis disequilibrium syndrome (DDS) is a clinical syndrome of neurologic deterioration resulting from cerebral edema seen in patients undergoing dialysis [[1]-[5]]. Although previous case series have documented increases in ICP via invasive monitoring during hemodialysis, particularly in patients with traumatic brain injury [[7], [25]], there is sparse evidence regarding ICP thresholds that may be necessary to undergo dialysis successfully without neurological sequelae in patients with DDS. Further reports correlating ICP responses to the volume of CSF drained in the peritoneal dialysis period are needed to delineate optimal CSF diversion in patients with DDS. [Extracted from the article]