Ibuprofen. I wonder how many doctors will try this in patients before human trials are proven. Ask your ER doctor
http://www.sciencedaily.com/releases/2012/10/121003111153.htm
Strokes often cause loss or impairment of vital brain
functions -- such as speech, movement, vision or attention. Restoration
of these functions is often possible, but difficult. One of the factors
impeding brain plasticity is inflammation. A study on rats, carried out
at the Nencki Institute in Warsaw, suggests that effectiveness of
neurorehabilitation after a stroke can be improved by anti-inflammatory
drugs.
Post-stroke inflammation slows down recovery and impairs brain
plasticity, reveal the results from the lab of Professor Małgorzata
Kossut at the Nencki Institute in Warsaw. The popular anti-inflammatory
drug ibuprofen restores the ability of brain cortex to reorganize -- a
process necessary for recovery of stroke-damaged functions.
"Our research was conducted on rats, but we have good reasons to
suppose that in future our results will help improve effectiveness of
rehabilitation of stroke patients," says Prof. Kossut.
The Nencki Institute team stresses that so far there are no proofs
that the treatment will be effective in humans and that they did not
investigate if the ibuprofen therapy prevents strokes, but concentrated
on post-stroke recovery.
The most frequent cause of stroke is blocking of brain arteries.
Without supply of oxygen, neurons die quickly. In the region of
stroke-induced damage pathological changes cause decrease of brain
tissue metabolism, impairment of neurotransmission and edema.
Brain control over physiological and voluntary functions may be lost,
depending on the localization of the infarct. Impairments of movement,
vision, speech and attention are frequent. In most cases these functions
return either partially or completely. Sometimes they return
spontaneously, more often after neurorehabilitation.
"In both instances recovery is based on neuroplasticity, the ability
of the brain to reorganize, that is to change the properties of neurons
and to alter the connections between them," says Dr. Monika
Liguz-Lęcznar (Nencki Institute).
After a stroke, neuroplasticity is impaired. Scientists from the
Nencki Institute suppose that this may be due to inflammation developing
at the site of the stroke. The proof that decreasing inflammation helps
neurorehabilitation came from experiments done on rats with
experimentally induced stroke. The stroke was localized in a special
region of the brain cortex, receiving information from whiskers.
The whiskers are important sensory organs of rodents, allowing the
animals to orient themselves in their environment in darkness. Every
whisker activates a small, precisely delineated chunk of brain cortex.
In healthy rats neuroplastic changes can be induced by cutting off
some of the whiskers, that is by eliminating part of the sensory input
to the brain. The brain reacts to that by letting the remaining whiskers
take over more cortical space, expand their cortical representation, at
the expense of the cut off ones.
"This plastic change does not occur when the site of stroke-induced
damage is near the region of cortex 'belonging' to the whiskers. We
showed that application of ibuprofen decreases inflammation and restores
neuroplasticity -- the brain cortex reorganizes like in healthy
animals," says Prof. Kossut.
The result obtained on rats indicates that ibuprofen (and probably
other anti-inflammatory medicines) may be beneficial in treating stroke
patients. Ibuprofen therapy should support brain plasticity by reducing
post-stroke inflammation and so speed up recovery of functions lost due
to the stroke. If the results on rats are verified in a proper clinical
trial, they may be influential in shaping the treatment of stroke
patients.
The research of Prof. Kossut's team on the effects of
anti-inflammatory drugs on neuroplasticity was funded by the
Polish-German Cooperation Program in Neuroscience and grants from the
Ministry of Science and Education.
Hmmm, I was told never to take Ibuprofen again.
ReplyDeleteThat was probably an outdated view and cya behavior
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