Mechanisms of neuroplasticity. Illustrated in panels (a)–(d) are the four primary mechanisms of neuroplasticity discussed in this review. (a) Plasticity hierarchy (adapted from Ius et al., 2011 [37
]). Areas in green have a high potential for plasticity while areas in red have a low potential for plasticity. Three lesion examples are illustrated in this figure. A lesion in the anterior frontal cortex (orange) would likely exhibit a high plasticity potential due to its noncritical role in complex higher-order functions. Conversely, a lesion in the posterior superior temporal gyrus (yellow; Wernicke’s area, a critical language network hub) or in the subcortical white matter tract (purple; inferior frontal occipital fasciculus, a major axonal pathway connecting receptive and expressive language areas) would be expected to have limited plasticity. (b) Cortical recruitment: when a cortical injury occurs (grey), perilesional synapses can be recruited to maintain synaptic integrity. (c) Cortical redundancy: redundant synapses are normally inhibited by interneurons (red shadow). Upon injury (grey), this inhibition is lost thus allowing for transmission of the redundant synapse. Instead of losing function, the redundant pathway compensates for the injured neurons. (d) Contralateral recruitment: a lesion (blue circle) in the hand motor area (green dashed region) can promote recruitment of the analogous contralateral hand area (green circle) to rescue hand function.