Cortical and network architectures in limb and oral apraxia

To characterize the distinct network principles underlying limb and oral apraxias, we investigated the structural brain lesions and white matter disconnections associated with limb apraxia (LA), buccofacial apraxia (BFA), and apraxia of speech (AOS) within a single cohort. In 136 patients with acute left-hemisphere ischemic stroke, LA was assessed using pantomime of tool use and communicative gestures, BFA via non-verbal orofacial movements, and AOS through perceptual evaluation of speech production tasks. We employed voxel-based, region-of-interest-based, and connectome-based lesion-symptom mapping to directly contrast the cortical damage and network disruptions associated with each deficit. LA was associated with damage to the inferior parietal lobule and widespread white matter disconnections within posterior networks, involving both intra-hemispheric and inter-hemispheric pathways. BFA was uniquely linked to an anterior lesion pattern centered on the ventral premotor cortex, driven by intrafrontal white matter disconnections. Furthermore, AOS emerged primarily as a focal cortical symptom linked to circumscribed lesions in the mid-precentral gyrus, with minimal structural disconnection. These findings demonstrate that LA emerges from disruptions within a widely distributed posterior network, whereas BFA involves an anterior intrafrontal network, contrasting with AOS which reflects a focal primary motor execution deficit. These data indicate that the neuroanatomical organization of apraxia is governed by the specific class of actions rather than simple effector specificity.