brain damage

#Three Stages to #COVID-19 #Brain Damage, New Review Suggests

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A new review outlines a three-stage classification of the impact of COVID-19 on the central nervous system and recommends hospitalized patients with the virus all undergo MRI to flag potential neurologic damage and inform postdischarge monitoring.

In stage 1, viral damage is limited to epithelial cells of the nose and mouth, and in stage 2 blood clots that form in the lungs may travel to the brain, leading to stroke. In stage 3, the virus crosses the blood–brain barrier and invades the brain.

“Our major take-home points are that patients with COVID-19 symptoms, such as shortness of breath, headache, or dizziness, may have neurological symptoms that, at the time of hospitalization, might not be noticed or prioritized, or whose neurological symptoms may become apparent only after they leave the hospital,” lead author Majid Fotuhi, MD, PhD, medical director of NeuroGrow Brain Fitness Center, McLean, Virginia, told Medscape Medical News.

“Hospitalized patients with COVID-19 should have a neurological evaluation and ideally a brain MRI before leaving the hospital; and, if there are abnormalities, they should follow up with a neurologist in 3 to 4 months,” said Fotuhi, who is also affiliate staff at Johns Hopkins Medicine in Baltimore, Maryland.

The review was published online June 8 in the Journal of Alzheimer’s Disease.

Wreaks CNS Havoc

It has become “increasingly evident” that SARS-CoV-2 can cause neurologic manifestations, including anosmia, seizures, stroke, confusion, encephalopathy, and total paralysis, the authors write.

The authors note that SARS-CoV-2 binds to angiotensin-converting enzyme 2 (ACE2) that facilitates the conversion of angiotensin II to angiotensin. After ACE2 has bound to respiratory epithelial cells, and then to epithelial cells in blood vessels, SARS-CoV-2 triggers the formation of a “cytokine storm.”

These cytokines, in turn, increase vascular permeability, edema, and widespread inflammation, as well as triggering “hypercoagulation cascades,” which cause small and large blood clots that affect multiple organs.

If SARS-CoV-2 crosses the blood–brain barrier, directly entering the brain, it can contribute to demyelination or neurodegeneration.

“We very thoroughly reviewed the literature published between January 1 and May 1, 2020 about neurological issues [in COVID-19] and what I found interesting is that so many neurological things can happen due to a virus which is so small,” said Fotuhi.

“This virus’ DNA has such limited information, and yet it can wreak havoc on our nervous system because it kicks off such a potent defense system in our body that damages our nervous system,” he said.

Three-Stage Classification

Stage 1

The extent of SARS-CoV-2 binding to the ACE2 receptors is limited to the nasal and gustatory epithelial cells, with the cytokine storm remaining “low and controlled.” During this stage, patients may experience smell or taste impairments, but often recover without any interventions.

Stage 2

A “robust immune response” is activated by the virus, leading to inflammation in the blood vessels, increased hypercoagulability factors, and the formation of blood clots in cerebral arteries and veins. The patient may therefore experience either large or small strokes.

Additional stage 2 symptoms include fatigue, hemiplegia, sensory loss, double vision, tetraplegia, aphasia, or ataxia.

Stage 3

The cytokine storm in the blood vessels is so severe that it causes an “explosive inflammatory response” and penetrates the blood–brain barrier, leading to the entry of cytokines, blood components, and viral particles into the brain parenchyma and causing neuronal cell death and encephalitis.

This stage can be characterized by seizures, confusion, delirium, coma, loss of consciousness, or death.

“Patients in stage 3 are more likely to have long-term consequences, because there is evidence that the virus particles have actually penetrated the brain, and we know that SARS-CoV-2 can remain dormant in neurons for many years,” said Fotuhi.

“Studies of coronaviruses have shown a link between the viruses and the risk of multiple sclerosis or Parkinson’s disease even decades later,” he added.

“Based on several reports in recent months, between 36% to 55% of patients with COVID-19 that are hospitalized have some neurological symptoms, but if you don’t look for them, you won’t see them,” Fotuhi noted.

As a result, patients should be monitored over time after discharge, as they may develop cognitive dysfunction down the road.

Additionally, “it is imperative for patients [hospitalized with COVID-19] to get a baseline MRI before leaving the hospital so that we have a starting point for future evaluation and treatment,” said Fotuhi.

“The good news is that neurological manifestations of COVID-19 are treatable,” and “can improve with intensive training,” including lifestyle changes—such as a heart-healthy diet, regular physical activity, stress reduction, improved sleep, biofeedback, and brain rehabilitation,” Fotuhi added.

Routine MRI Not Necessary

Kenneth Tyler, MD, chair of the Department of Neurology at the University of Colorado School of Medicine, disagreed that all hospitalized patients with COVID-19 should routinely receive an MRI.

“Whenever you are using a piece of equipment on patients who are COVID-19 infected, you risk introducing the infection to uninfected patients,” he told Medscape Medical News.

Instead, “the indication is in patients who develop unexplained neurological manifestations — altered mental status or focal seizures, for example —because in those cases, you do need to understand whether there are underlying structural abnormalities,” said Tyler, who was not involved in the review.

Also commenting on the review for Medscape Medical News, Vanja Douglas, MD, associate professor of clinical neurology, University of California San Francisco, described the review as “thorough” and suggested it may “help us understand how to design observational studies to test whether the associations are due to severe respiratory illness or are specific to SARS-CoV-2 infection.”

Douglas, who was not involved in the review, added that it is “helpful in giving us a sense of which neurologic syndromes have been observed in COVID-19 patients, and therefore which patients neurologists may want to screen more carefully during the pandemic.”

The study had no specific funding. Fotuhi has disclosed no relevant financial relationships. Coauthor Cyrus Raji reports consulting fees as a member of the scientific advisory board for Brainreader ApS and reports royalties for expert witness consultation in conjunction with Neurevolution LLC. Tyler and Douglas have disclosed no relevant financial relationships.

#Brain damage reversed in a drowned toddler

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Subacute normobaric and hyperbaric oxygen therapy restored drowning-induced cortical grey matter and white matter loss.

In what is believed to be a world first, a team of US doctors are reporting a case of reversal of brain damage in a two-year-old child who experienced cardiac arrest after cold water drowning.

In February 2016, the child wandered into the family swimming pool and was submerged in 5°C water for up to 15 minutes. Four days after the incident, MRI showed deep grey matter injury. Cerebral atrophy and grey and white matter loss were observed on day 32. She was discharged home on day 35, unresponsive to all stimuli, immobile with legs drawn to her chest, and with constant squirming and head shaking.

From day 56, normobaric oxygen was administered twice daily. Hyperbaric oxygen therapy (HBOT) was introduced on day 79. Presenting the case in the journal Medical Gas Research , the authors say neurological improvements were observed on initiating each therapy. After HBOT, the patient demonstrated normal speech and cognition, assisted gait, with residual fine motor and temperament deficits. MRI 27 days after HBOT showed near-normalisation of ventricles and reversal of atrophy.

The authors attribute the “startling regrowth of tissue” to the fact that they were able to intervene early in a growing child, before long-term tissue degeneration.

Teenagers who smoke cannabis damage their brains for LIFE and may be more likely to develop schizophrenia

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  • U.S. study found that mice exposed to even small doses of marijuana for 20 days suffered lasting brain damage into adulthood
  • Results highlight how teenagers who regularly smoke weed may have a greater risk of developing schizophrenia

Teenagers who regularly smoke cannabis suffer long lasting brain damage and are in much greater danger of developing schizophrenia.

American researchers say the drug is particularly dangerous for a group of people who have a genetic susceptibility to the mental health disorder – and it could be the trigger for it.

Asaf Keller, of the University of Maryland School of Medicine, said the results highlight the dangers of teenagers smoking cannabis during their formative years.


The study found that even short-term exposure to cannabis impaired brain activity, with the damage continuing into adulthood

The study, published in the journal Neuropsychopharmacology, exposed young mice to the active ingredient in marijuana for 20 days.

It found that their brain activity was impaired, with the damage continuing into adulthood.

The past 20 years has seen major controversy about the long-term effects of marijuana, with experts divided over its long-term effects on teenagers.

Previous research has shown that children who started using marijuana before the age of 16 are at greater risk of permanent brain damage, and have a significantly higher incidence of psychiatric disorders.

‘Adolescence is the critical period during which marijuana use can be damaging,’ said the study’s lead author, Sylvina Mullins Raver, a PhD candidate at the University of Maryland School of Medicine.

‘We wanted to identify the biological underpinnings and determine whether there is a real, permanent health risk to marijuana use.’

The scientists began by examining cortical oscillations in mice. Cortical oscillations are patterns of the activity of neurons in the brain and are believed to underlie the brain’s various functions.

These oscillations are very abnormal in schizophrenia and in other psychiatric disorders.



The scientists exposed young mice to very low doses of the active ingredient in marijuana for 20 days, and then allowed them to return to their siblings and develop normally.

‘In the adult mice exposed to marijuana ingredients in adolescence, we found that cortical oscillations were grossly altered, and they exhibited impaired cognitive abilities,’ said Raver.

‘We also found impaired cognitive behavioural performance in those mice. The striking finding is that, even though the mice were exposed to very low drug doses, and only for a brief period during adolescence, their brain abnormalities persisted into adulthood.’

The scientists repeated the experiment, this time giving marijuana to adult mice that had never been exposed to the drug before.

Cannabis use

According to the research team, there is a group of people who have a genetic susceptibility to developing schizophrenia. Adding weed to the mix during adolescence could be the trigger that causes it to develop, permanently impairing brain function and cognition

Their cortical oscillations and ability to perform cognitive tasks remained normal, indicating that it was only drug exposure during the critical teenage years that impaired brain activity.

‘We found that the frontal cortex is much more affected by the drugs during adolescence,’ said Keller.
‘This is the area of the brain controls executive functions such as planning and impulse control. It is also the area most affected in schizophrenia.’

Keller now wants to know whether the effects can be reversed. ‘We are hoping we will learn more about schizophrenia and other psychiatric disorders, which are complicated conditions,’ he said.

‘These cognitive symptoms are not affected by medication, but they might be affected by controlling these cortical oscillations.’


 A separate study by Imperial College London last month revealed that long-term use of cannabis destroys dopamine, the feel-good chemical in the brain that inspires a spirit of get-up-and-go.

Previous research has suggested taking marijuana can lead to individuals becoming withdrawn, lethargic and apathetic.

The cannabis users in the study published in Biological Psychiatry had all experienced psychotic-like symptoms while smoking the drug such as strange sensations or having feelings of paranoia.

The researchers expected their dopamine production might be higher since this has been linked with psychosis – but instead found the opposite.

The cannabis users had their first experience with the drug between the ages of 12 and 18 and the researchers believe the drug could be the cause of the difference in dopamine levels.

‘Cannabis is an illegal drug and there is mounting evidence the idea of it being a harmless herb is not true,’ said Dr Michael Bloomfield, of Imperial College London.

‘When people stop taking cannabis it seems the brain can slowly go back to producing pretty normal levels of dopamine.

‘Cannabis has effects on the brain and it’s important people can make an informed decision.’

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Treatment with halogen mitigates brain damage after cardiac arrest

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Inhaling xenon gas combined with hypothermia results in less white matter damage, Finnish study finds.

Patients experiencing cardiac arrest out-of-hospital could benefit from a treatment with a halogen gas. According to the results of a Finnish study published in “JAMA”, treating comatose survivors of out-of-hospital cardiac arrest with inhaled xenon gas combined with hypothermia resulted in less white matter damage.

For the study, the researchers at the University of Turku, Finland randomly assigned 110 successfully resuscitated, but still comatose patients who had experienced an out-of-hospital cardiac arrest to receive either inhaled xenon combined with hypothermia for 24 hours or hypothermia treatment alone. The trial was conducted at two intensive care units in Finland.

MRI data from 97 patients was collected a median of 53 hours after cardiac arrest, showing that patients in the xenon group had less white matter damage compared to the control group.

There was no significant difference in neurological outcomes or death at six months; however, the study was not powered for this, the researchers noted, adding that the preliminary findings require further evaluation in an adequately powered clinical trial designed to assess clinical outcomes.