At what point does the sleep loss you have post-stroke start causing problems? And what is your doctor doing to prevent those problems? Do drugs to sleep exacerbate or solve the problem?
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The longer the insomnia, junctions of cerebral blood vessels begin to degrade
In search of the answer to why do we sleep, research conducted at the
Mexican Metropolitan Autonomous University (UAM) revealed that chronic
sleep loss can cause certain neurotoxic molecules, which normally
circulate in the blood, to be transported to the central nervous system
and interfere with the function of neurons.
Beatriz Gómez González, professor and researcher at UAM and head of
the scientific project, explained that this phenomenon arises due to an
alteration in the central nervous system called blood-brain barrier,
which is the component responsible for protecting the brain from
potentially neurotoxic agents.
Through the induction of sleep loss on some animals, the specialist
at UAM and his staff corroborated that the longer the period of
insomnia, joints vessels in the blood-brain barrier began to degrade.
"The blood vessels were found not so closely united, we observed that
some elements could cross that barrier and reach the brain tissue
itself," explained the researcher.
By entering the brain, some nerve agents could potentially affect
neuronal function and even promote neuron death. For example, the
specialist said, an agent called monosodium glutamate found in a wide
range of processed foods may cause neuronal damage by overactivation of
these cells (excitotoxicity), although the range of neurotoxic agents
circulating in the blood is very extensive.
Furthermore, the research group at UAM studied the risks that could
arise as a result of the administration of some drugs to the increased
permeability of the blood-brain barrier induced by chronic sleep loss.
Gómez González said that, based on some studies, it has been confirmed
that some second-generation antihistamines permeate into the brain
tissue when this phenomenon occurs.
"Although manufacturers of antibiotic drugs or second-generation
antihistamines ensure that these do not affect brain function, there is
evidence that these may impact on the central nervous system when there
is an increase in the permeability of the blood-brain barrier," said the
researcher. This phenomenon may cause some unwanted excitotoxicity
effects in neurons, drowsiness, behavioral changes and even neuronal
death.
Another phenomenon reported by researchers at UAM, with the induction
of sleep loss in animals is the increased number of pinocytotic
vesicles in cells. These relate to certain folds of a cell elements and
capture materials found in the bloodstream; but this phenomenon may
increase the risk of neurotoxic elements entering the brain tissue. "The
animals that have been induced sleeplessness develop up to three times
these vesicles compared to animals in natural state."
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