Apathy is a reduction in motivated goal-directed behavior (GDB) that is prevalent in cerebrovascular disease, providing an important opportunity to study the mechanistic underpinnings of motivation in humans. Focal lesions, such as those seen in stroke, have been crucial in developing models of brain regions underlying motivated behavior, while studies of cerebral small vessel disease (SVD) have helped define the connections between brain regions supporting such behavior. However, current lesion-based models cannot fully explain the neurobiology of apathy in stroke and SVD. To address this, we propose a network-based model which conceptualizes apathy as the result of damage to GDB-related networks. A review of the current evidence suggests that cerebrovascular disease-related pathology can lead to network changes outside of initially damaged territories, which may propagate to regions that share structural or functional connections. The presentation and longitudinal trajectory of apathy in stroke and SVD may be the result of these network changes. Distinct subnetworks might support cognitive components of GDB, the disruption of which results in specific symptoms of apathy. This network-based model of apathy may open new approaches for investigating its underlying neurobiology, and presents novel opportunities for its diagnosis and treatment.

冷漠是脑血管疾病中普遍存在的动机性目标导向行为（GDB）的减少，为研究人类动机的机械基础提供了重要机会。局灶性病变（例如中风中的病变）对于开发动机行为基础的大脑区域模型至关重要，而对脑小血管疾病（SVD）的研究已帮助定义了支持此类行为的大脑区域之间的联系。但是，当前基于病变的模型无法完全解释中风和SVD的冷漠神经生物学。为了解决这个问题，我们提出了一个基于网络的模型，该模型将无动于衷的概念归结为对GDB相关网络的破坏。对当前证据的回顾表明，与脑血管疾病有关的病理可能导致最初受损的区域之外的网络变化，并可能传播到共享结构或功能连接的区域。中风和SVD的冷漠表现和纵向轨迹可能是这些网络变化的结果。不同的子网可能支持GDB的认知成分，其破坏会导致特定的冷漠症状。这种基于网络的冷漠模型可能会为研究其潜在的神经生物学开辟新的方法，并为其诊断和治疗提供了新的机会。不同的子网可能支持GDB的认知成分，其破坏会导致特定的冷漠症状。这种基于网络的冷漠模型可能会为研究其潜在的神经生物学开辟新的方法，并为其诊断和治疗提供了新的机会。不同的子网可能支持GDB的认知成分，其破坏会导致特定的冷漠症状。这种基于网络的冷漠模型可能会为研究其潜在的神经生物学开辟新的方法，并为其诊断和治疗提供了新的机会。