Deficits in the ability to draw objects, despite apparently intact perception and motor abilities, are defined as constructional apraxia. Constructional deficits, often diagnosed based on performance on copying complex figures, have been reported in a range of pathologies, perhaps reflecting the contribution of several underlying factors to poor figure drawing. The current study provides a comprehensive analysis of brain–behavior relationships in drawing disorders based on data from a large cohort of subacute stroke patients ( n = 358) using whole-brain voxel-wise statistical analyses linked to behavioral measures from a complex figure copy task. We found that (i) overall poor performance on figure copying was associated with subcortical lesions (BG and thalamus), (ii) lateralized deficits with respect to the midline of the viewer were associated with lesions within the posterior parietal lobule, and (iii) spatial positioning errors across the entire figure were associated with lesions within visual processing areas (lingual gyrus and calcarine) and the insula. Furthermore, deficits in reproducing global aspects of form were associated with damage to the right middle temporal gyrus, whereas deficits in representing local features were linked to the left hemisphere lesions within calcarine cortex (extending into the cuneus and precuneus), the insula, and the TPJ. The current study provides strong evidence that impairments in separate cognitive mechanisms (e.g., spatial coding, attention, motor execution, and planning) linked to different brain lesions contribute to poor performance on complex figure copying tasks. The data support the argument that drawing depends on several cognitive processes operating via discrete neuronal networks and that constructional problems as well as hierarchical and spatial representation deficits contribute to poor figure copying.

This study is the first to assess lesion–symptom relations for subitizing and counting impairments in a large sample of neuropsychological patients (41 patients) using an observer-independent voxel-based approach. We tested for differential effects of enumerating small versus large numbers of items while controlling for hemianopia and visual attention deficits. Overall impairments in the enumeration of any numbers (small or large) were associated with an extended network, including bilateral occipital and fronto-parietal regions. Within this network, severe impairments in accuracy when enumerating small sets of items (in the subitizing range) were associated with damage to the left posterior occipital cortex, bilateral lateral occipital and right superior frontal cortices. Lesions to the right calcarine extending to the precuneus led to patients serially counting even small numbers of items (indicated by a steep response slope), again demonstrating an impaired subitizing ability. In contrast, impairments in counting large numerosities were associated with damage to the left intraparietal sulcus. The data support the argument for some distinctive processes and neural areas necessary to support subitization and counting with subitizing relying on processes of posterior occipital cortex and with counting associated with processing in the parietal cortex.