Thursday, 29 October 2020

Corona! I Barely Know Her! Learning To Live With A Treacherous Partner

Today's post from (see link below) is an important one for people already living with neuropathy and other neurological disorders and then being confronted with Covid-19. It shows us that far from being at the end, or even in the middle of a new viral pandemic, we're actually at the very beginning of what may be a long learning curve with as yet unknown physical problems as the virus attacks our immune systems. As understanding of the virus increases, we're already learning that there are several different forms of Covid-19 and they seem to affect people randomly across the age groups. You may have heard about 'long' covid for instance, where recovered patients may need to live the rest of their lives with debilitating side effects but that may be just the tip of the iceberg. The medical world doesn't understand yet why it happens!

This article reveals the virus' potential for damaging the brain (and thus our nervous systems) but yet again, the disease is so young, there's a mountain of information yet to be learned and understood and in that respect, only time will tell how damaging the virus will be. One thing is sure; as new, daily evidence emerges, neuropathy patients may end up being in the front line of side effects sufferers as our immune systems adapt to attacks from covid-19. People living with autonomic neuropathy already know how wide ranging nerve damage can be in disrupting our bodily functions. Covid may be about to bring a whole new range of neurological problems into the spotlight. Be alert and keep your doctor informed. He or she may not yet be aware of covid's affects on the nervous system, so it's up to us to do our research and provide evidence from that research, so that our physicians are at least aware of potential neurological problems and can work through our recovery together.


How COVID-19 can damage the brain

Some people who become ill with the coronavirus develop neurological symptoms. Scientists are struggling to understand why.
View through the bottom of a laboratory dish being held by a scientist containing brain organoids seen as small white dots

Some evidence that SARS-CoV-2 can infect the brain comes from ‘organoids’ — clumps of neurons created in a dish. Credit: Erik Jepsen/UC San Diego

The woman had seen lions and monkeys in her house. She was becoming disoriented and aggressive towards others, and was convinced that her husband was an impostor. She was in her mid-50s — decades older than the age at which psychosis typically develops — and had no psychiatric history. What she did have, however, was COVID-19. Hers was one of the first known cases of someone developing psychosis after contracting the disease1.

In the early months of the COVID-19 pandemic, doctors struggled to keep patients breathing, and focused mainly on treating damage to the lungs and circulatory system. But even then, evidence for neurological effects was accumulating. Some people hospitalized with COVID-19 were experiencing delirium: they were confused, disorientated and agitated2. In April, a group in Japan published3 the first report of someone with COVID-19 who had swelling and inflammation in brain tissues. Another report4 described a patient with deterioration of myelin, a fatty coating that protects neurons and is irreversibly damaged in neurodegenerative diseases such as multiple sclerosis.

“The neurological symptoms are only becoming more and more scary,” says Alysson Muotri, a neuroscientist at the University of California, San Diego, in La Jolla.

The list now includes stroke, brain haemorrhage and memory loss. It is not unheard of for serious diseases to cause such effects, but the scale of the COVID-19 pandemic means that thousands or even tens of thousands of people could already have these symptoms, and some might be facing lifelong problems as a result.

Yet researchers are struggling to answer key questions — including basic ones, such as how many people have these conditions, and who is at risk. Most importantly, they want to know why these particular symptoms are showing up.

Although viruses can invade and infect the brain, it is not clear whether SARS-CoV-2 does so to a significant extent. The neurological symptoms might instead be a result of overstimulation of the immune system. It is crucial to find out, because these two scenarios require entirely different treatments. “That’s why the disease mechanisms are so important,” says Benedict Michael, a neurologist at the University of Liverpool, UK.

Affected brains

As the pandemic ramped up, Michael and his colleagues were among many scientists who began compiling case reports of neurological complications linked to COVID-19.

In a June paper5, he and his team analysed clinical details for 125 people in the United Kingdom with COVID-19 who had neurological or psychiatric effects. Of these, 62% had experienced damage to the brain’s blood supply, such as strokes and haemorrhages, and 31% had altered mental states, such as confusion or prolonged unconsciousness — sometimes accompanied by encephalitis, the swelling of brain tissue. Ten people who had altered mental states developed psychosis.

Not all people with neurological symptoms have been seriously ill in intensive-care units, either. “We’ve seen this group of younger people without conventional risk factors who are having strokes, and patients having acute changes in mental status that are not otherwise explained,” says Michael.

A physiotherapist wearing protective clothing assists a patient suffering from Covid-19 in a hospital in France

Neurological symptoms accompanying COVID-19 include delirium, psychosis and stroke.Credit: Stephane Mahe/Reuters

A similar study1 published in July compiled detailed case reports of 43 people with neurological complications from COVID-19. Some patterns are becoming clear, says Michael Zandi, a neurologist at University College London and a lead author on the study. The most common neurological effects are stroke and encephalitis. The latter can escalate to a severe form called acute disseminated encephalomyelitis, in which both the brain and spinal cord become inflamed and neurons lose their myelin coatings — leading to symptoms resembling those of multiple sclerosis. Some of the worst-affected patients had only mild respiratory symptoms. “This was the brain being hit as their main disease,” says Zandi.

Less common complications include peripheral nerve damage, typical of Guillain–BarrĂ© syndrome, and what Zandi calls “a hodgepodge of things”, such as anxiety and post-traumatic stress disorder. Similar symptoms have been seen in outbreaks of severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS), also caused by coronaviruses. But fewer people were infected in those outbreaks, so less data are available.

How many people?

Clinicians don’t know how common these neurological effects are. Another study6 published in July estimated their prevalence using data from other coronaviruses. Symptoms affecting the central nervous system occurred in at least 0.04% of people with SARS and in 0.2% of those with MERS. Given that there are now 28.2 million confirmed cases of COVID-19 worldwide, this could imply that between 10,000 and 50,000 people have experienced neurological complications.

But a major problem in quantifying cases is that clinical studies have typically focused on people with COVID-19 who were hospitalized, often those who required intensive care. The prevalence of neurological symptoms in this group could be “more than 50%”, says neurobiologist Fernanda De Felice at the Federal University of Rio de Janeiro in Brazil. But there is much less information about those who had mild illness or no respiratory symptoms.

That scarcity of data means it is difficult to work out why some people have neurological symptoms and others do not. It is also unclear whether the effects will linger: COVID-19 can have other health impacts that last for months, and different coronaviruses have left some people with symptoms for years.

Infection or inflammation?

The most pressing question for many neuroscientists, however, is why the brain is affected at all. Although the pattern of disorders is fairly consistent, the underlying mechanisms are not yet clear, says De Felice.

Finding an answer will help clinicians to choose the right treatments. “If this is direct viral infection of the central nervous system, these are the patients we should be targeting for remdesivir or another antiviral,” says Michael. “Whereas if the virus is not in the central nervous system, maybe the virus is clear of the body, then we need to treat with anti-inflammatory therapies.”

Getting it wrong would be harmful. “It’s pointless giving the antivirals to someone if the virus is gone, and it’s risky giving anti-inflammatories to someone who’s got a virus in their brain,” says Michael.

There is clear evidence that SARS-CoV-2 can infect neurons. Muotri’s team specializes in building ‘organoids’ — miniaturized clumps of brain tissue, made by coaxing human pluripotent stem cells to differentiate into neurons.

In a May preprint7, the team showed that SARS-CoV-2 could infect neurons in these organoids, killing some and reducing the formation of synapses between them. Work by immunologist Akiko Iwasaki and her colleagues at Yale University School of Medicine in New Haven, Connecticut, seems to confirm this using human organoids, mouse brains and some post-mortem examinations, according to a preprint published on 8 September8. But questions remain over how the virus might reach people’s brains.

Because loss of smell is a common symptom, neurologists wondered whether the olfactory nerve might provide a route of entry. “Everyone was concerned that this was a possibility,” says Michael. But the evidence points against it.

A team led by Mary Fowkes, a pathologist at the Icahn School of Medicine at Mount Sinai in New York City, posted a preprint in late May9 describing post mortems in 67 people who had died of COVID-19. “We have seen the virus in the brain itself,” says Fowkes: electron microscopes revealed its presence. But virus levels were low and were not consistently detectable. Furthermore, if the virus was invading through the olfactory nerve, the associated brain region should be the first to be affected. “We’re simply not seeing the virus involved in the olfactory bulb,” says Fowkes. Rather, she says, infections in the brain are small and tend to cluster around blood vessels.

Michael agrees that the virus is hard to find in the brain, compared with other organs. Tests using the polymerase chain reaction (PCR) often do not detect it there, despite their high sensitivity, and several studies have failed to find any virus particles in the cerebrospinal fluid that surrounds the brain and spinal cord (see, for example, ref. 10)10. One reason might be that the ACE2 receptor, a protein on human cells that the virus uses to gain entry, is not expressed much in brain cells10.

“It seems to be incredibly rare that you get viral central nervous system infection,” Michael says. That means many of the problems clinicians are seeing are probably a result of the body’s immune system fighting the virus.

Still, this might not be true in all cases, which means that researchers will need to identify biomarkers that can reliably distinguish between a viral brain infection and immune activity. That, for now, means more clinical research, post mortems and physiological studies.

De Felice says that she and her colleagues are planning to follow patients who have recovered after intensive care, and create a biobank of samples including cerebrospinal fluid. Zandi says that similar studies are beginning at University College London. Researchers will no doubt be sorting through such samples for years. Although the questions they’re addressing have come up during nearly every disease outbreak, COVID-19 presents new challenges and opportunities, says Michael. “What we haven’t had since 1918 is a pandemic on this scale.”

Nature 585, 342-343 (2020)


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    Paterson, R. W. et al. Brain (2020).

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    Kotfis, K. et al. Crit. Care 24, 176 (2020).

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    Moriguchi, T. et al. Int. J. Infect. Dis. 94, 55–58 (2020).

  4. 4.

    Zanin, L. et al. Acta Neurochir. 162, 1491–1494 (2020).

  5. 5.

    Varatharaj, A. et al. Lancet Psychiatry (2020).

  6. 6.

    Ellul, M. A. et al. Lancet Neurol. 19, 767–783 (2020).

  7. 7.

    Mesci, P. et al. Preprint at bioRxiv (2020).

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    Song, E. et al. Preprint at bioRxiv (2020).

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    Bryce, C. et al. Preprint at medRxiv (2020).

  10. 10.

    Al Saiegh, F. et al. J. Neurol. Neurosurg. Psychiatry 91, 846–848 (2020).

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    Li, M.-Y., Li, L., Zhang, Y. & Wang, X.-S. Infect. Dis. Poverty 9, 45 (2020).

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Tuesday, 13 October 2020

The Decisions And Diagnoses Current Covid-19 Patients May Need To Understand

 Today's post from (see link below) may not be directly linked to covid-19 and nerve damage but pretty successfully tries to highlight the dilemmas doctors are facing when confronted with this new virus. As patients, with or without direct symptoms of Corona, we have to put our trust in the doctors who treat us, their treatment plans and their conclusions but we're rarely privy to the decision difficulties doctors themselves face. Corona is new for them too and very few will sit their patients down and explain all the ins and outs of something they barely understand themselves, so we have to try to find basic information for ourselves and we all know how the internet can be a minefield when it comes to diseases with no fast and certain rules (in that respect, very familiar for neuropathy patients). This article more or less sets out what the current understanding of Covid-19 is and how it's currently being treated. For that reason alone, it's very useful for the confused and scared patient, seeking clear information from reliable sources. That said, this virus is still in its infancy and changes its parameters almost every week and that's before we start talking about potential mutations, with all the uncertainty they bring. All we can do is trust the basic information that is available this week but for the future, we have to enter the maze side by side with the doctors - it's a mutual journey of discovery and we can only hope that the science stays a few steps ahead of the virus and we come out healthy on the other side. This article will provide you with some reliable and trustworthy information but be prepared for it all to change as the viral snowball hurtles down the hill!

What We’ve Learned About Treating COVID

photo of ventilator

  This past spring, health care providers at hospitals around the country scrambled to treat people who were critically ill with a virus they’d only just heard of themselves. Usually, when a severely ill person arrives at the hospital, doctors already know or can quickly find established guidelines, based on years of research, for treating the sickness. But in the spring of 2020, nothing was established about COVID-19.

“It was a dramatic situation. We had a lot of sick people, in a very short period of time, and it was overwhelming to take care of them. There was an almost irrational exuberance to try any treatment that we could think of,” says David Kaufman, MD, director of medical intensive care at New York University Langone Health in New York City.

While doctors may have at times rushed to try anything, that trial and error over the last 6 months has helped accumulate the scientific evidence of what works and what doesn’t in the treatment of COVID-19.

“The ability of the medical community to pull together quickly to get these large critical care studies done in a very short period of time with reliable, high-quality results is amazing,” Kaufman says. “It’s like being in a wartime economy when all automobile and refrigerator factories convert to make tanks and planes.”

The Case for Steroids

At the start of the pandemic, doctors didn’t have a go-to medication they could give to critically sick COVID-19 patients admitted to their ERs and ICUs. Today, corticosteroids are that medication. Last week, on the heels of several scientific studies that supported the move, the World Health Organization (WHO) released its official recommendation that people with severe COVID-19 receive steroids to improve their chances of survival.

“Low-dose steroids for 10 days or until the patient is discharged, whichever one comes first, can actually help with symptoms, can avoid escalating to a ventilator, and can lower the risk of death,” says Javier Lorenzo, MD, a critical care anesthesiologist at Stanford Hospital and Clinics in Stanford, CA.

That’s because steroids act as anti-inflammatories. The worst cases of COVID-19 are marked by extreme inflammation that doesn’t let up. A little inflammation at the beginning of a viral infection helps fight it off. But in serious cases of COVID-19, the inflammation gets out of control and can eventually lead to organ failure and death.

“Steroids may not be good for people who have only had the infection for a few days because they may actually limit the body’s ability to fight infection,” Kaufman says. “But in people who are critically ill because of over-inflammation, steroids help put a lid on it.”

Growing Evidence for Remdesivir

In May, the FDA authorized hospitals to give remdesivir to adults and children with severe COVID-19. In late August, the agency expanded that authorization to anyone hospitalized with the virus.

In a study of 1,063 adults in the hospital with COVID-19, the ones who got remdesivir recovered in about 11 days compared to about 15 for those who got a placebo.

“This data is not quite as robust as it is for steroids,” Lorenzo says, “but we know that patients who get remdesivir can experience faster resolution of symptoms, shorter duration of hospitalization, and be less likely to need a ventilator.”

Controversy Over Convalescent Plasma

Also in late August, the FDA granted health care providers emergency use authorization for convalescent plasma in the treatment of COVID-19.

Plasma is the part of the blood that carries antibodies against viruses. In this case, the treatment uses plasma donated by survivors of COVID-19. The idea is that COVID-19 survivors have antibodies that fight the virus. Through plasma, doctors can pass those virus-fighting antibodies onto others struggling to fight the illness.

The concept dates back to at least the 1918 Spanish flu pandemic. But it’s unclear just how helpful it is in COVID-19. There hasn’t been a large, randomized, controlled clinical trial to compare the effects of convalescent plasma to placebo. Some trials are currently enrolling volunteers.

“The evidence for convalescent plasma is really weak,” Lorenzo says. “Not all plasma is equal. Not all plasma has high titers [high concentration of antibodies], and not all antibodies neutralize the virus. We’re using it, but it’s still not clear whether it’s effective or not.”

To Intubate or Not

Some critical care doctors may be holding off on intubating patients and putting them on a mechanical ventilator a little longer than they did earlier in the pandemic. Intubation requires heavy sedation and care in the ICU. Early in the pandemic, when doctors saw that patients were progressing in their need for oxygen, many erred on the side of caution and put patients on a ventilator sooner rather than later.

At the time, before doctors knew the benefits of steroids and remdesivir, the thought was that the patient would escalate and eventually need the ventilator no matter what.

“So if we did it early, rather than waiting until it was an emergency, when we could take our time donning the personal protective equipment, we would also reduce the risk of exposure to our health care workers,” Lorenzo says.

Doctors were also concerned that oxygen delivered through a tube in the nose – a step below a mechanical ventilator -- could push the virus out into the air and increase exposure risk for health care workers, too.

“But we now know that in some patients, if we give the steroids and remdesivir a little bit more time, and allow them to escalate a little further along with high-flow nasal [oxygen], we might just squeak by and not have to put them on a ventilator,” Lorenzo says.

In Stanford’s ICU, Lorenzo says, they are now confident their staff are protected. “The risk of aerosolization of the virus is real. But we now know that our health care provider infection rate is low. So if we maintain our full PPE guidelines, then the risk of transmission is low, and we might be able to prevent the patient from escalating to a ventilator.”

New research shows this may be a safe risk to take. A recent study found that there was no difference in survival rates among COVID-19 patients who went directly on a ventilator and those who were put on nasal oxygen first.

Prone to Recover Faster

Some patients on ventilators may recover faster by spending some time each day lying prone, or face down. It doesn’t work for everyone. But for those who benefit, the idea is that the face-down position may distribute oxygen more evenly throughout the lungs. Long before COVID-19, critical care providers flipped sedated patients on ventilators onto their stomachs in order to get more oxygen into their lungs.

But since the pandemic, some ICUs are trying it on patients who are awake and perhaps on the way to needing a ventilator. Numerous clinical trials in progress are examining the benefits for patients who are not yet on a ventilator but struggling to get oxygen.

“For some patients, the oxygen level goes up, but it’s not universal,” Kaufman says. “And soon after you stop lying on your stomach, the oxygen goes back down.”

Unprecedented Collaboration

On the road to finding what works, health care providers have thrown out many things that proved not to work, too.

“A lot of people were talking about hydroxychloroquine,” Lorenzo says. “But we now know, unequivocally, that we shouldn’t be using it. It doesn’t work. And it probably can cause more harm than good.”

They’ve learned what works and what doesn’t more quickly through unprecedented collaboration with their co-workers and frontline health care workers around the globe.

Under “normal” circumstances, researchers tightly guard data until it is published. “Now, some of these trials may release unpublished data if they feel that the benefit is real and substantial,” Lorenzo says.

Social media groups for critical care doctors, he says, are also more active than ever.

Kaufman is part of an email chain with pulmonologists and critical care doctors from all over the world. Many are in Europe and got intensive experience with COVID-19 months ahead of doctors in the U.S. “To be connected with some of the worldwide masters in mechanical ventilation who are at some of the hardest hit cities in the world is an amazing privilege. It’s like sitting at the foot of Sophocles, learning from the ancient masters,” he says.

But for all they’ve learned, much is still unknown. Doctors still don’t understand why some patients get through the virus after a week of mild symptoms while others escalate to a ventilator in the same amount of time. “We still don’t know how patients progress in this disease,” Lorenzo says.

But after a frenzied springtime in which many health care providers tried anything that might work, Lorenzo says, “We have learned from this pandemic that we can’t relax our scientific rigor. We have to abide by the same process of peer-reviewed clinical trials that we normally do or we can harm patients.”

WebMD Health News Reviewed by Michael W. Smith, MD on September 10, 2020


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Friday, 2 October 2020

The Beast That Is Chronic Pain: What Is That Exactly?

 Today's post comes from an excellent and very informative American article from (see link below) concerning the nature of pain. Now readers of this blog will generally only be interested in information that covers neuropathic (nerve) pain but neuropathic pain is rarely the only form of pain you feel when you have nerve damage and most importantly, people living with nerve damage can (and often do) have other pain-causing problems too. It's vital that you can identify the nature of your discomfort - where it comes from and how best to treat it but even seasoned doctors have diagnosis difficulties with neuropathy and identifying whether your pain is acute or chronic, where it stems from and which of the more than 100 forms of neuropathy might be causing it. Believe me, if you've had the same pain problems for more than 2 or 3's chronic! But that's only the beginning of your treatment story when it comes to nerve damage. This article is aimed at an American audience but apart from local and specific other influences, the information applies across the world.What it does is helps you sort out the wheat from the chaff so to speak and helps you understand the nature of your pain, so that you can better concentrate on the right treatment. Well worth a read, for beginning neuropathy patients, pain sufferers and those more experienced who are still floundering in the mass of information that can be thrown at you. Take your time; it's a long article but worth the effort.
Chronic Pain in the US                         John Ryan,  J.Flowers Health Institute,  2020
Chronic pain (long-term pain) affects about 40 million people in the US.
Some sources say the numbers could be as high as 100 million. Beyond the debilitating personal effects, chronic pain costs the US over $600 billion every year.
Pain is a subjective experience. What’s painful to one person might be just a slight discomfort to another. That said, pain that lasts for long periods could be crippling, regardless of its severity.
People in the US report having more pain than people in other countries. 1 in 3 Americans reports that they experience pain “often” or “very often.” In Croatia, the proportion is only 1 in 10 people. This is according to the International Social Survey Program.
In the US, 126.1 million adults had experienced some pain in the past three months. Among them, 10.5 million had experienced severe pain every day.4
In 2013, 178 million Americans aged 18 years and older had at least one painful condition. This was up from 120.2 million in 1997.5

What Is Pain?

The International Association for the Study of Pain (IASP) defines pain as
“An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”6
In layman’s terms, pain is an experience that causes discomfort. It may be due to an injury or to the brain’s inability to process pain signals properly. Pain may vary in severity, location, and the involvement of body parts.
Some pain may be limited to the area of injury, while some pain may affect the entire body. A headache involves only the head, and a stomachache affects only the belly.
People use different terms to describe their pain. Some of them include: