Neural plasticity often has a favorable connotation when described in the context of recovery of function. However, plasticity can also serve to impede behavioral change. Interference refers to the ability of plasticity within a given neural circuitry to impede the induction of new, or expression of existing, plasticity within that same circuitry. This, in turn, can impair learning. Although some types of noninvasive cortical stimulation applied during or shortly before skill training may enhance motor learning, other forms can be disruptive of learning. For example, transcranial direct current stimulation given after training reduced the training-dependent increases in cortical excitability . Similarly, swallowing function can be
both enhanced and impaired by peripheral stimulation, as discussed in Robbins et al.Rodent experiments of spatial learning have shown that saturation of synaptic potentiation within the hippocampus, a brain structure critical for spatial learning, impairs subsequent learning . Presumably, synchronizing training with stimulation improves performance because the behavioral signals driving plasticity during training are augmented by the presence of the extra stimulation. When stimulation is applied outside of the training experience, in addition to potentially disrupting the memory consolidation process, it may induce plasticity
that is not shaped by behavioral signals and is, therefore, detrimental to performance. This has specific implications for how adjuvant stimulation might be applied
to enhance recovery after brain damage. It is also possible for behavioral experience to drive
plasticity within residual brain areas in a direction that will impede optimal behavioral recovery. Brain damage survivors may develop compensatory strategies that are
easier to perform (“bad habits”) than more difficult but ultimately more effective strategies acquired through rehabilitation. These strategies might be adopted earlier and used with much greater frequency than those guided in therapy. The ease of learning certain compensatory
behaviors may also be facilitated after brain damage. After small unilateral sensorimotor cortex lesions, rats have a reduction in apparent aiming errors when learning a new skilled reaching task with the less-affected forelimb compared with intact rats, and this is related to
enhanced neuroplastic changes in the contralesional motor cortex ual lesions of the motor cortex also enhance some function in the ipsilesional hand . However, over-reliance on less-affected modalities may also exaggerate impairments. Early skill training that was focused on the ipsilesional limb of rats with unilateral infarcts was found to greatly worsen subsequent performance and decreased use of the impaired forelimb , suggesting that it contributed to learned nonuse . When maladaptive, these selftaught compensatory strategies may induce plasticity that will have to be overcome with subsequent rehabilitation
and other treatment approaches . Another reason to consider interference effects is that a therapy that benefits one skill may interfere with performance of another. Furthermore, as brain injury may change the neural response during learning, it may also change sensitivities to interference effects. For example, providing explicit instruction on how to perform a
motor sequence task was found to improve implicit motor learning in healthy controls, whereas the same instructions interfered with learning in subjects with strokes