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These studies suggest that during a stroke, the brain experiences cell death due to excitotoxicity, oxidative stress, and apoptosis, disrupts connectivity leading to motor impairments, and undergoes a period of neuroplasticity that can be influenced by rehabilitation.
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During a stroke, the brain undergoes a series of complex and damaging processes. The primary mechanisms include excitotoxicity, oxidative and nitrative stress, inflammation, and apoptosis. Excitotoxicity occurs when excessive glutamate release leads to overactivation of receptors, causing an influx of calcium ions that damage neurons. Oxidative stress results from the overproduction of free radicals, which further harm cellular structures. Inflammation exacerbates brain injury by disrupting the blood-brain barrier and promoting cell death. Apoptosis, or programmed cell death, is another critical pathway leading to neuronal loss .
Following the initial injury, the brain enters a state of heightened plasticity, which is crucial for recovery. This period allows for the sprouting of new axons, formation of new synapses, and remapping of sensory-motor functions. These changes are driven by molecular systems similar to those involved in learning and memory, such as alterations in cellular excitability. This plasticity is essential for motor recovery and is being targeted in clinical trials to develop new stroke recovery drugs .
Stroke not only affects the immediate area of the brain where the injury occurred but also disrupts functional brain networks. Neuroimaging studies have shown that stroke leads to changes in connectivity between different brain regions, both near and far from the lesion site. This reorganization is crucial for recovery, as it involves restoring interhemispheric functional coherence and enhancing top-down control over motor areas. These network changes are associated with both impairments and recovery of motor functions .
In addition to localized inflammation at the injury site, stroke can trigger a global inflammatory response throughout the brain. This widespread inflammation can exacerbate secondary brain injury by damaging the blood-brain barrier, causing microvascular failure, and inducing further neuronal death. Understanding the mechanisms behind this global inflammation is essential for developing therapeutic strategies to mitigate its effects and improve long-term outcomes for stroke patients.
A stroke initiates a cascade of damaging processes in the brain, including excitotoxicity, oxidative stress, inflammation, and apoptosis. However, the brain's remarkable plasticity and ability to reorganize its networks offer pathways for recovery. Advances in understanding these mechanisms are paving the way for new therapeutic interventions aimed at enhancing brain repair and functional recovery post-stroke.
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