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Synchronization of brain activity fluctuations is believed to representcommunication between spatially distant neural processes. These inter-arealfunctional interactions develop in the background of a complex network ofaxonal connections linking cortical and sub-cortical neurons, termed the human"structural connectome". Theoretical considerations and experimental evidencesupport the view that the human brain can be modeled as a system operating at acritical point between ordered (sub-critical) and disordered (super-critical)phases. Here, we explore the hypothesis that pathologies resulting from braininjury of different etiology are related to the model of a critical brain. Forthis purpose, we investigate how damage to the integrity of the structuralconnectome impacts on the signatures of critical dynamics. Adopting a hybridmodeling approach combining an empirical weighted network of human structuralconnections with a conceptual model of critical dynamics, we show that lesionslocated at highly transited connections progressively displace the modeltowards the sub-critical regime. The topological properties of the nodes andlinks are of less importance when considered independently of their weight inthe network. We observe that damage to midline hubs such as the middle andposterior cingulate cortex is most crucial for the disruption of criticality inthe model. However, a similar effect can be achieved by targeting lesstransited nodes and links whose connection weights add up to an equivalentamount. This implies that brain pathology does not necessarily arise due toinsult targeted at well-connected areas and that inter- subject variabilitycould obscure lesions located at non-hub regions. Finally, we discuss thepredictions of our model in the context of clinical studies of traumatic braininjury and neurodegenerative disorders.

Dynamical signatures of structural connectivity damage to a model of the brain posed at criticality