![]() ![]() ![]() ![]() Finally, this framework was used to predict the physiological correlates of paradoxical lesions. This paradoxical lesion effect disappeared when the second lesion was more severe because plasticity-related changes were disproportionately amplified in the intrinsic connectivity, relative to lesioned extrinsic connections. We found that when the second lesion was mild, there was an increase in experience-dependent plasticity that enhanced performance relative to a single lesion. The second lesion was implemented in the intrinsic (within region) connectivity, compromising the model’s ability to rebalance excitatory–inhibitory connections during learning. The first in-silico lesion simulated damage to the extrinsic (between regions) connectivity causing a functional deficit that did not fully resolve over 100 trials of a word repetition task. For this, we introduce in-silico lesions to an active inference model of auditory word repetition. In this article, we simulate how and when a modification of the excitatory–inhibitory balance triggers the reversal of a functional deficit caused by a primary lesion. This effect has been explained in several ways particularly by the reduction of functional inhibition, or by increases in the excitatory-to-inhibitory synaptic balance within perilesional tissue. Paradoxical lesions are secondary brain lesions that ameliorate functional deficits caused by the initial insult. ![]()
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