Key Points Reductions in blood flow to the brain of sufficient duration and extent lead to stroke, which results in damage to neuronal networks and impairment of sensation, movement or cognition. A time-limited window of neuroplasticity opens following stroke in the adult brain, during which partial behavioural recovery can occur. Neuroplasticity can be further augmented by rehabilitative therapy. Enhanced sensory and motor performance that occur after stroke is referred to as recovery, although re-emergent post-stroke behaviour is unlikely to be identical to the pre-stroke state. A more accurate definition of recovery is behavioural compensation provided by remaining and newly developed brain circuits that results in altered and/or new response strategies. Plasticity in the adult brain after stroke is enabled by a surprising amount of diffuse and redundant connectivity in the CNS and the ability of new structural and functional circuits to form through remapping between related cortical regions. Many of the molecular mechanisms that underlie stroke recovery are identical to those involved in development. A 'critical period' of heightened neuroplasticity that is akin to that occurring during visual system development might exist after stroke. For successful rehabilitation after stroke it is crucial to align behavioural interventions with critical periods. It is possible to conceptualize synaptic learning rules after stroke into two broad classes and temporal phases: first, homeostatic mechanisms ensure that each neuron receives an adequate amount of synaptic input akin to homeostatic plasticity; second, Hebbian mechanisms occur, during which synaptic strength is redistributed to favour coincident activity and properly functioning circuits.
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Biomedicine,general,Neurosciences,Behavioral Sciences,Biological Techniques,Neurobiology,Animal Genetics and Genomics