Category Archives: Neurology

Darius Settles was sent home from the emergency room twice after contracting COVID-19 in June. The first time, he was told to come back if his condition worsened. On his second visit, his blood-oxygen levels were normal enough to discharge him again. He died in July, the youngest person killed by the coronavirus in Nashville, Tennessee, at that time.

Situations in which patients seem better, get discharged, then see their conditions worsen, have become common over the course of the pandemic. New research suggests it may be related to infections in the brain.

"People seem to have very nice recovery, lung functions are fine, and we send them home just to find out that three days later, the patient becomes so severe that they died," Mukesh Kumar, a virologist at Georgia State University, told Insider. "That usually can only happen when the brain is involved."

Kumar recently published a study in the journal Viruses that examines how COVID-19 affects the brains of mice.

His results showed that three days after the mice were infected with the coronavirus, they displayed high levels of virus in their lungs. By days five and six, their lungs had started to clear up but their brains showed about 1,000 times more virus than the peak levels found in the lungs. That coincided with the arrival of severe symptoms such as labored breathing, disorientation, and weakness.

The virus also triggered an inflammatory response in the brain, marked by the release of chemical signals called cytokines. Under normal circumstances, cytokines tell the immune system to fight off infection but too many cytokines can instruct the body to attack its own cells, triggering dangerous levels of inflammation. The mice brains in the study showed around 10 to 50 times more cytokines than the lungs.

In some mice, the reaction caused immediate death. But in mice with milder cases, the virus seemed to hide out in the brain indefinitely.

Though results of mice studies don't always hold true for humans, Kumar suspects that the brain is a major target for the coronavirus.

"Our brain doesn't have that good immune response like our lungs or our heart, so whenever the virus goes in the brain, it can replicate very well," Kumar said. "It can stay there for a long time."

Viral replication in the brain could also explain why some coronavirus patients have persistent neurological issues, such as dizziness or brain fog, long after they've tested negative for COVID-19. In some cases, Kumar said, there's a risk these neurological problems may give rise to chronic illnesses such as autoimmune disorders, Parkinson's, or multiple sclerosis.

"Depending upon your immune response or antibody levels, it could cause low levels of inflammation, or maybe make you prone to other disease, or maybe reactivate later," he said. "All these are still outstanding questions because we are still only one year into the pandemic."

A woman improperly wears her face mask in Rome, Italy, on April 29, 2020. Andreas Solaro/AFP/Getty Images

COVID-19 is often described as a respiratory disease, since the coronavirus attacks the lungs first. But some researchers suspect it may be a vascular disease, given that some patients develop blood clots, leaky capillaries, and inflamed blood vessels, which can lead to heart damage or stroke.

ADutch study of 184 coronavirus patients in the ICU found that nearly one-third of patients had blood clots. And aJuly study of 100 COVID-19 patients found that 78 of them had some degree of heart damage. Studies have also suggested that nearly 2% of COVID-19 patients have strokes far more than than the rate of strokes among influenza patients.

But Kumar's study didn't detect any virus in the blood of infected mice.

Instead, his research showed that the virus entered the brain through the nasal passages, before attacking the central nervous system. Part of that nervous system controls our sense of smell, which may explain why many coronavirus patients have trouble smelling. Kumar said it's possible that the virus could reach the brain after entering the mouth as well, but the nose is a more direct pathway.

In mice, the coronavirus seemed to have trouble replicating in organs such as the heart, liver, or kidneys. But an infection in the brain can ultimately damage such organs, Kumar said.

"It doesn't even have to go to every organ, because if it can go to the brain, there are several parts of the brain that control all other organs," he said. "So it could also be possible that you don't even need virus in the lungs to cause lung failure."

A patient who has recovered from COVID-19, gestures next to his son as he leaves the Juarez Hospital in Mexico City, Mexico, July 27, 2020. Edgard Garrido/Reuters

Neurological issues are more common among coronavirus patients than scientists originally thought.

An October study found that 82% of coronavirus patients admitted to a hospital network in Chicago in March and April 2020 had neurological symptoms. The issues ranged from relatively minor headaches, dizziness, and loss of smell to serious conditions like brain damage, strokes, and seizures.

In some cases, these symptoms can linger for at least several months.

A recent study from University of Oxford researchers, which is still awaiting peer review, found that 13% of people who got COVID-19 were diagnosed with a psychiatric or neurological illness within six months of testing positive for the virus. Some patients even showed signs of Parkinson's disease or Guillain-Barr syndrome, a rare autoimmune disorder, but those results weren't statistically significant.

Kumar said it's fairly simple to tell whether a patient has a severe neurological condition, since the issue will likely show up on an MRI or CT scan. But mild neurological problems are often difficult to pinpoint.

"Unfortunately, based on other studies, it could be lifelong," Kumar said. "We know patients who are still showing symptoms who were infected a year ago."

The research he did on mouse brains, however, is difficult to replicate in humans.

"The patient has to die to actually find out if the virus is hiding in the brain," he said.

Originally posted here:
COVID-19 can hide in the brains of mice, cause neurological issues - Business Insider - Business Insider

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The Telegraph

Ursula von der Leyen on Monday pinned the blame for the vaccine fiasco that led Brussels to threaten a hard border on the island of Ireland on her trade commissioner Valdis Dombrovskis. The European Commission president threw her deputy, who leads DG Trade, under the bus amid rising anger from EU capitals at her go it alone tactics during last weeks battle with AstraZeneca. Jean-Claude Juncker, Mrs von der Leyen's predecessor, said he was "very much opposed" to her export restriction measures. In a speech in Stuttgart on Sunday, Mr Juncker also said of the EUs vaccine procurement: "It all went too slow, it all should have been done more transparently, even though that would have been difficult." This regulation falls under the responsibility of Mr Dombrovskis, said Eric Marmer, the European Commissions chief spokesman, referring to the former prime minister of Latvia, a Brussels veteran with a reputation for caution. In my country we have a saying, Only the Pope is infallible. Mistakes can happen along the way the important thing is that you recognise them early on, Mr Mamer said. Alexander Stubb, the former prime minister of Finland who campaigned to be appointed European Commission, president was scathing about Mrs Von der Leyen. He said "Number one rule of any leader: if your organisation screws up; never, ever blame your team publicly" Mrs von der Leyen was forced into a humiliating climbdown on Friday after announcing Brussels would trigger Article 16 of the Northern Ireland Protocol, to prevent AstraZeneca vaccines being smuggled into Britain from Northern Ireland. The move, which was announced without notifying Ireland or Britain, would have created a vaccine border after years of Brexit talks to avoid a hard border on the island. After the Irish prime minister called Mrs von der Leyen, the regulation, which could have facilitated a vaccine export ban to non-EU countries including Britain, was amended. Mr Mamer said that the regulation to create an export transparency mechanism, which including the Article 16 measure, was passed provisionally and at speed by the entire College of Commissioners on Friday. Asked by the Telegraph if this was Ms Van der Leyens worst week, he said: We believe that we are on the right track since the beginning of this pandemic in ensuring there is as cohesive and as effective a European response as possible. Mrs von der Leyens attempts to pass the buck cut no ice with EU diplomats, who suggested she had gone rogue, or German MPs in Berlin, who plan to summon Ursula von der Leyen for questioning. In a further blow to Mrs von der Leyen, the move was led by MPs from her own party, Angela Merkel's Christian Democrats (CDU). Mrs von der Leyen has refused calls for a public debate on the debacle in the European Parliament. Instead she will on Tuesday hold closed door meetings with MEPs with parties who approved her appointment. It is understood that Mrs von der Leyen took personal charge of the vaccine row and that DG Trades senior official is Sabine Weyand, whose objections to triggering Article 16 were reported to have been overruled. Ms Weyand is keenly aware of the political sensitivities around the Brexit divorce treatys Northern Ireland Protocol. She was Michel Barniers deputy Brexit negotiator and a key figure in the creation of the Irish border backstop.

More:
VCA Animal Referral & Emergency Center of Arizona has a neurology department that can treat a variety of conditions - Yahoo News

Reviewed This Month

Effect of Out-of-Hospital Tranexamic Acid vs. Placebo on 6-Month Functional Neurologic Outcomes in Patients With Moderate or Severe Traumatic Brain Injury.

Authors: Rowell SE, Meier EN, McKnight B, et al.

Published in: JAMA, 2020 Sep 8; 324(10): 96174. Erratum in: JAMA, 2020 Oct 27; 324(16): 1,683.

Over the last decade, the use of tranexamic acid (TXA) for traumatic hemorrhage control has increased. This was due to the results of a clinical trial, published in 2010, that found early administration of TXA was a cost-effective way to reduce the risk of death in bleeding trauma patients.

Further research has shown that TXA is safe for patients with traumatic brain injury (TBI). In this months Journal Watch, we review a randomized, double-blind multicenter trial designed to examine the efficacy and safety of out-of-hospital administration of tranexamic acid compared to placebo in participants with moderate or severe TBI who were not in shock.

The objective of this trial was to determine whether TXA administered by EMS within two hours of injury improved neurologic outcome. Read that objective carefullyit will be important when putting the results of this trial into context.

Neurologic outcome was measured using the Glasgow Outcome Score-Extended (GOSE). The authors chose to dichotomize this scale into favorable (which included moderate disability or good recovery) and poor (which included severe disability, vegetative state, or death) outcomes.

The authors also examined many secondary outcomes, including 28-day mortality, six-month disability, progression of intracranial hemorrhage, incidence of neurosurgical interventions, hospital-free days, ICU-free days, incidence of seizures, and incidence of thrombotic events, to name a few.

The study was conducted in 12 regions across the U.S. and Canada. It included 39 EMS agencies and 20 trauma centers. To be eligible for enrollment in this trial, patients had to be at least 15 years of age, with moderate or severe blunt or penetrating TBI, a GCS score of 3 to 12, at least one reactive pupil, a systolic blood pressure of at least 90 mm Hg, and an IV in place prior to randomization.

Participants were randomized into one of three treatment groups. The first received a 1-gram IV bolus of TXA by EMS followed by a gram of in-hospital TXA infused over eight hours. The next group received a 2-gram TXA bolus by EMS followed by a placebo infusion. The final group received an IV bolus placebo by EMS and a placebo infusion in the hospital. Study kits that appeared identical were shipped to participating EMS agencies for placement on EMS vehicles in random order. Each vehicle only carried one study kit at a time.

The study was conducted between May 2015 and March 2017 under U.S. regulations for exception from informed consent and the Canadian tricouncil policy statement on ethical conduct in research involving humans.

There were 966 patients included in the analysis. Their average age was 42, and almost three-quarters (74%) were male. The average GCS score was 8. The three study groups were similar when comparing demographics and baseline anatomic and physiologic characteristics as well as injury severity. However, the authors note there were fewer penetrating injuries in the bolus-only group.

The median estimated time from injury to EMS administration of the study drug ranged from 40 to 43 minutes. The median time from EMS administration to the start of the in-hospital infusion ranged from 86 to 96 minutes.

The evaluation of the primary study outcome, favorable or poor neurologic function, revealed no statistically significant difference when comparing TXA to placebo (65% vs. 62%, p=0.16). Therefore, the conclusion of this study was that among patients with moderate or severe TBI, out-of-hospital tranexamic acid administration within two hours of injury did not improve six-month neurologic outcome as measured by the GOSE.

However, as we discuss often in this column, we should not let statistical significance alone guide our judgment of importance. There was a 3% difference in favorable neurologic outcome. While that difference may not be statistically significant, could it be clinically meaningful?

Now, rather than simply read the objective and conclusion of this paper, lets dive a little deeper. As mentioned earlier, the authors also examined several secondary outcomes. When evaluating 28-day mortality, the TXA groups showed a 3% improvement (14% vs. 17%). This result was also not statistically significant, with a p-value of 0.26.

There was also an 8% difference in 28-day mortality when comparing the bolus-only group to the placebo group for those patients with intracranial hemorrhage. This difference was statistically significant (p=0.03). The total number of adverse events was also similar between groups.

Why would the authors report such a cut-and-dried conclusion when there seems to be a trend favoring the use of TXA? Well, the authors indicate in their methods section that the study was specifically designed to evaluate neurologic outcomes at six months. This was specified in the original trial registry on ClinicalTrials.gov. The authors had to stick to the primary outcome that was specified prior to the beginning of trial enrollment for the resulting manuscript.

However, the authors are clear that we should carefully interpret their findings. They state in their discussion that despite no statistically significant difference in the primary outcome in either trial, there were important differences and findings from both trials that warrant consideration and future investigation.

In other words, the results seem to be trending in a favorable direction when EMS administers TXA early. So, rather than to simply conclude from these findings that TXA is not effective in the treatment of TBI, an important next step would be to design studies that specifically evaluate outcomes other than the dichotomous GOSE score at six months.

As with all studies there are limitations here. There were some difficulties in obtaining follow-up data six months after the injury. This is not surprising, given that patients were enrolled prior to giving consent. There was also a low percentage of patients with intracranial hemorrhage enrolled in the study. This may have diluted the treatment differences.

This was a very well done study that will lead to further analysis of TXA administration. It is also a great example of how we should avoid letting a p-value alone guide our judgment of importance.

I hope you have an opportunity to read the manuscript yourself. There are many other interesting results that could not fit into this months Journal Watch. And, as always, I hope to review your study in an upcoming edition soon.

Antonio R. Fernandez, PhD, NRP, FAHA, is a research scientist at ESO and an assistant professor in the department of emergency medicine at the University of North CarolinaChapel Hill. He is on the board of advisors of the Prehospital Care Research Forum at UCLA.

Read this article:
Journal Watch: TXA and Neuro OutcomesMore Than Meets the Eye - EMSWorld

An investigation looks at the neurological manifestations of COVID-19.

Although coronavirus disease 2019 (COVID-19) is first and foremost a respiratory disease, the past year has shown that the disease can also impact other systems in the body, particularly the cardiovascular system. A report in TheLancet Children & Adolescent Health looks at how the disease shows up in neuroimaging.1

The researchers put out an international call to find cases of children who had encephalopathy that was linked to a severe case of COVID-19. They asked for the clinical history as well as association cerebrospinal fluid and plasma data for each case as well. Each case was looked at by a child neurologist, pediatric infectious disease expert, and central neuroradiology panel. Any case that did not have a direct link to a COVID-19 infection was excluded from the study.

A total of 38 children with neurological disease linked to COVID-19 were found in France, the United Kingdom, the United States, Brazil, Argentina, India, Peru, and Saudi Arabia. The researchers found recurring patterns of disease and the neuroimaging abnormalities seen ranged from mild to severe. The most common neuroimaging patterns found were postinfectious immune-mediated acute disseminated encephalomyelitis-like changes of the brain (16 patients), neural enhancement (13 patients), and myelitis (8 patients). Children with multisystem inflammatory syndrome in children were the ones most likely to have splenial lesions (7 patients) and myositis (4 patients). Complications in the cerebrovascular system were not as common among children and adults. No significant pre-existing conditions were seen in children and most of them had favorable outcomes. Four children who previously been healthy before COVID-19 developed fatal atypical central nervous system co-infections.

The researchers concluded that central nervous system abnormalities have been seen in children who had COVID-19. They urged further research to get a better understanding of how the disease can impact the central nervous system as well as provide information on how to provide long-term follow-up care.

Reference

1. Lindan C, Mankad K, Ram D, et al. Neuroimaging manifestations in children with SARS-CoV-2 infection: a multinational, multicentre collaborative study. Lancet Child Adolesc Health. December 15, 2020. Epub ahead of print. doi:10.1016/S2352-4642(20)30362-X

Read more:
Examining the neurological manifestations of COVID-19 - Contemporary Pediatrics

NEW YORK, Jan. 26, 2021 /PRNewswire/ --Soterix Medical Inc. (SMI), the global leader in non-invasive stimulation and synergistic brain imaging technologies, announces a new clinical trial of home-based auricular Vagus Nerve Stimulation (taVNS) for individuals who experience post-COVID neuropsychiatric symptoms, like fatigue, headache, or anxiety. The trial involves an innovative, first-of-its kind home-based neuromodulation solution that combines Soterix Medical's unique wearable taVNS platform, with ElectraRx portal for remote stimulation control, and home-based vital sign monitoring.

Emerging studies show COVID can affect patients during two distinct phases of the disease process: the acute stage, characterized by fever, heart or lung problems, and the post-COVID phase, in which neuropsychiatric symptoms, like fatigue, anxiety and depression, can occur.

Researchers have used the term "neuroCOVID" to describe when the second phase is characterized by one or a combination of neuropsychiatric symptoms like vertigo, loss of smell, headaches, fatigue and irritability as well as anxiety and depression. Some studies estimate one in five COVID patients will develop these long-term symptoms.

The study is supported in part by the National Institutes of Health-funded Delaware Clinical and Translational Research Program to address neuroCOVID symptoms in patients. The trial is designed around a unique technology suite that combines precise vagus nerve stimulation with real-time remote-control as well as remote physiological sensing by the clinical team. The trial is based on the established anti-inflammatory response to vagus nerve stimulation.

Mr. Kamran Nazim, Chief Product Manager of Soterix Medical adds, "This study will leverage our unparalleled expertise in developing noninvasive technologies to stimulate the vagus nerve. Soterix Medical has over a decade of experience designing and deploying the more reliable, targeted, and intelligent non-invasive brain stimulation devices. Our proprietary remote-controlled taVNS system is uniquely optimized for this novel indication."

Ms. Claudia Giselle, Soterix Medical's VP Regulatory Affairs, adds "In addition to Soterix Medical's unique wearable vagus nerve stimulation platform, this trial integrates technology for telemedicine support including video and real-time home-based blood pressure, pulse and oxygen saturation levels. The sophistication of this integrated system is a testament to our commitment to provide the most advanced stimulation and integrated monitoring technologies, for the most important medical indications of our time."

CAUTION: Soterix Medical taVNS platform is limited by Federal (or United States) law to investigational use only.

Media Contact: Mariana Shuster Tel: +1-888-990-8327 Email: [emailprotected]

SOURCE Soterix Medical Inc.

Read this article:
Soterix Medical study to address post-COVID neurological and psychiatric symptoms using at-home neuromodulation and monitoring - PRNewswire