Apraxia is frequently described after left hemisphere stroke and results from lesions to a complex network for motor cognition with dorso-dorsal, ventro-dorsal and ventral processing streams. Apraxia also occurs after right hemisphere stroke, but lesion correlates and underlying mechanisms remain to be elucidated.

To clarify the role of the right hemisphere in apraxic deficits and the influence of neglect, we prospectively examined apraxia (imitation of meaningless postures and pantomime of tool use) and neglect in 138 acute right hemisphere stroke patients with first-ever ischemic stroke in the middle cerebral artery territory and identified corresponding lesion correlates using voxel-based lesion-symptom mapping.

Imitation of meaningless postures was impaired as frequently as after left hemisphere stroke (38.4%) and was significantly associated with neglect. Imitation of meaningless postures was related to temporal (middle temporal gyrus, temporoparietal junction, superior temporal gyrus and sulcus), parietal (angular gyrus, parieto-occpitpial sulcus), secondary sensorimotor cortex and (peri-)insular lesions. Presence of neglect dichotomized the results: a lesion correlate for isolated imitation without neglect was found in the right parieto-occipital cortex, while imitation deficits, when co-occurring with neglect, were related to lateral occipito-temporal, superior temporal sulcus and (peri-)insular lesions. Pantomime of tool use deficits, typical for apraxia after left hemisphere lesions, were found in only 5 cases (3.6%) and only in the context of neglect, and were associated with occipital lobe, ventral and anterior temporal lobe, and inferior frontal (areas 45/47) lesions.

The syndrome of apraxia after right hemisphere stroke differs from apraxia after left hemisphere stroke. Imitation deficits are found in both hemispheres after dorso-dorsal stream lesions. Neglect also leads to and explains deficits in imitation and pantomime in patients with right ventral stream lesions. Therefore, in right hemisphere lesions, apraxia can either be explained as impaired visuomotor transformation or as a result of visuospatial deficits.

左半球卒中后经常描述失用症，其原因是病变形成复杂的网络，通过背-背，腹-背和腹侧加工流进行运动认知。右半球卒中后也发生失用症，但病变相关，其潜在机制尚待阐明。

为了弄清右半球在肢体缺损中的作用和忽视的影响，我们前瞻性检查了138例中度首次缺血性卒中的急性右半球卒中患者的失用症（模仿无意义的姿势和使用工具的手势）使用基于体素的病变症状图谱，将脑动脉区域和已识别的相应病变关联起来。

模仿无意义的姿势与左半球卒中后一样频繁（38.4％）受损，并且与忽视有关。模仿无意义的姿势与颞（中颞回，颞顶交界，颞上回和沟），顶（角回，顶-枕沟），继发的感觉运动皮层和（周围）病变有关。忽视的存在将结果分为两部分：在右侧顶枕皮层中发现了与孤立模仿无关的病变相关的病变，而与忽略同时发生时，模仿缺陷与外侧枕颞，颞上沟和（周围）有关-）岛状病变。仅在5例中发现了典型的工具使用缺陷手势，这种缺陷通常发生在左半球病变后的失用症中（3。

右半球卒中后的失用症候群不同于左半球卒中后的失用症。背-背流损伤后在两个半球都发现了模仿缺陷。忽视也导致并解释了右腹侧流病变患者模仿和哑剧的缺陷。因此，在右半球病变中，失用症可以解释为视运动转换受损或视空间缺陷的结果。