Characterising factors underlying praxis deficits in chronic left hemisphere stroke patients.

Limb apraxia, a disorder of skilled action not consequent on primary motor or sensory deficits, has traditionally been defined according to errors patients make on neuropsychological tasks. Previous models of the disorder have failed to provide a unified account of patients' deficits, due to heterogeneity in the patients and tasks used. In this study we hypothesised that we may be able to map apraxic deficits onto principal components, some of which may be specific, whilst others may align with other cognitive disorders. We implemented principal component analysis (PCA) to elucidate core factors of the disorder in a preliminary cohort of 41 unselected left hemisphere chronic stroke patients who were tested on a comprehensive and validated apraxia screen. Three principal components were identified: posture selection, semantic control and multi-demand sequencing. These were submitted to a lesion symptom mapping (VBCM) analysis in a subset of 24 patients, controlled for lesion volume, age and time post-stroke. The first component revealed no significant structural correlates. The second component was related to regions in inferior frontal gyrus, primary motor area, and adjacent parietal opercular (including inferior parietal and supramarginal gyrus) areas. The third component was associated with lesions within the white matter underlying the left sensorimotor cortex, likely involving the 2nd branch of the left superior longitudinal fasciculus as well as the posterior orbitofrontal cortex (pOFC). These results highlight a significant role of common cognitive functions in apraxia, which include action selection, and sequencing, whilst more specific deficits may relate to semantic control. Moreover, they suggest that previously described 'ideomotor' and 'ideational' deficits may have a common neural basis within semantic control. Further research using this technique would help elucidate the cognitive processes underlying limb apraxia, its neural correlates and their relationship with other cognitive disorders.