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ShareOct. 3, 2012 — 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.
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The above story is reprinted from materials provided by Nencki Institute of Experimental Biology.
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