Wearing face masks do no harm
The principal mode of SARS-CoV-2 transmission
involves viral entry through the respiratory tract. This generally
occurs when an infected individual coughs, sneezes, or speaks,
generating aerosols carrying the virus. At the onset of the pandemic,
there was rudimentary knowledge about the virus, and policies were
developed based on the best available evidence. Thus, guidelines
regarding wearing face masks differed among countries and over time. At
present, scientists are convinced that masks are paramount in reducing
viral spread.
As the pandemic ravages the world relentlessly, there
has been a setback in government measures to contain the virus globally.
A large number of protestors have taken to the streets against the
compulsory use of face masks. They have condemned mandatory mask-wearing
as "an infringement of freedom", "violation of religious
rights", or a part of a broader conspiracy that "COVID-19 is a
hoax". Some have proclaimed that mask-wearing engenders"more harm
than good" due to rebreathing CO2, with some even considering that
"masks are lethal."
Researchers at Florida recruited 15 house-staff
physicians without any pulmonary conditions and 15 patients with COPD.
They monitored their EtCO2 and SpO2 throughout the time they were
wearing surgical masks, and arterial blood gases before and after a
6-minute walking test with masks on. They found that gas exchange was
not significantly affected by the use of masks, even in those with
severe lung impairment. They feel that dyspnea experienced by some
people wearing masks does not stem from hypercarbia or hypoxemia;
rather, it occurs from a restriction of airflow, especially when higher
ventilation is needed on exertion.
This research, although small, dispels some
misconceptions surrounding the use of face masks in the context of the
surging COVID-19 pandemic.
(Annals of the American Thoracic Society 2 October
2020)
Classical music improves epilepsy: The Mozart effect
Epilepsy is a common disorder, affecting
approximately 0.64% of the world population, resulting in substantial
neurologic, cognitive, psychological, and social consequences. Treatment
frequently involves multi-drug therapy, but seizures persist in about
30% of them. Among the non-pharmacological approaches for drug-resistant
epilepsy, there is an evolving interest in non-invasive forms of
neurostimulation such as music therapy. A recent meta-analysis has shown
that listening to Mozart’s piano music can reduce the frequency of
epilepsy.
The music compositions of Wolfgang Amadeus Mozart
date way back to the 18th century. It was in 1993 that Francis Rauscher
claimed that listening to Mozart’s music improved the spatiotemporal
senses of normal subjects. However, clinicians have always treated the
‘Mozart Effect’ with some scepticism.
More recently, two Italian researchers, Gianluca
Sesso and Federico Sicca, systematically reviewed existing research
works and found that listening to Mozart led to a remarkable decrease in
epileptic seizures (31%–66%) and interictal epileptiform discharges.
These effects occurred after a single music session and were sustained
after a prolonged treatment duration. Sonatas for two pianos, K448 and
K545, had an exceptionally positive effect. The researchers believe that
Mozart’s sonatas might have distinctive rhythmic structures specifically
suited to working on epilepsy.
The highly congruous results of this meta-analysis
firmly imply that Mozart’s music could be an effective non-invasive
method for improving clinical outcomes in epilepsy, especially in
difficult-to-treat ones. Nevertheless, the exact mechanisms of the
Mozart effect on the brain should be understood to use this method in
clinical settings.
(European College of Neuropsychopharmacology Congress
September 2020, Clinical Neurophysiology April 2020)
SARS-CoV-2 spike protein allays pain
A group of researchers based at the University of
Arizona Health Sciences have reported that SARS-CoV-2 spike protein
could relieve pain.
Numerous biological pathways signal the human body to
perceive pain, one among which is the vascular endothelial growth
factor-A (VEGF-A)/neuropilin signaling pathway. VEGF-A binds to the
receptor neuropilin and kicks off a cascade of events causing neuronal
hyperexcitability and resulting in pain.
Neuropilin-1 is the second receptor proposed for
SARS-CoV-2 in some studies; angiotensin converting enzyme-2 being the
first. The research team found that the SARS-CoV-2 spike protein binds
to neuropilin at the same location as VEGF-A, thereby hindering VEGF-A
from binding to it. In a series of experiments in the laboratory and in
rodent models, spike protein reversed VEGF-A induced pain signaling.
This research finding could perhaps explain how
SARS-CoV-2 reduces pain in some patients and stays under the radar.
According to the U.S. Centers for Disease Control and Prevention, 50% of
COVID-19 transmission occurs before symptom onset and 40% of infections
are asymptomatic. This research also paves the way to explore a novel
class of non-opioid therapeutics for pain targeting the VEGF-A/neuropilin
pathway that would reduce opioid abuse.
This finding could have important implications at a
time we arewaging a war against the COVID-19 pandemic and the opioid
epidemic.
(PAIN 1 October 2020)