Meaningless imitation in neurodegenerative diseases: Effects of body part, bimanual imitation, asymmetry, and body midline crossing

Visuo-imitative apraxia has been consistently reported in patients with dementia, yet there have been substantial methodological differences between studies, while multiple, sometimes competing hypotheses have been put forward to explain this syndrome. Our goals were to study specific imitation deficits in groups of patients who have been selected and assigned to a group solely based on clinical criteria. We tested the effects of body part, bimanual imitation, asymmetry of the model, and body midline crossing, in patients with cortical atrophy of the temporal lobes (semantic dementia, SD), frontal-parietal networks (FPN, i.e., posterior cortical atrophy and corticobasal syndrome) or both (Alzheimer's disease, AD). Sixty-three patients and 32 healthy controls were asked to imitate 45 meaningless finger/hand, uni-/bimanual, asymmetrical/symmetrical, and crossed/uncrossed postures. SD patients had subnormal imitation scores. FPN patients showed frequent and marked deficits in most conditions, better performance with hand than finger postures (probably because of visuo-constructive deficits), and better performance with uncrossed than crossed configurations (probably because of body schema disorganization). Bimanual configurations were difficult for AD patients, not because of bimanual activity in itself, but rather because of the complexity of the model. The finding of dissociations in 34/63 cases (54%) suggests that some patients, even within the same clinical category, can have variable performance in imitation tests as a function of the abovementioned factors. Clinicians are advised to use tests with a large array of items to properly capture patients' imitation skills. This provides a new basis for future research to unpack which neurocognitive mechanisms are disrupted to cause specific patterns of impaired imitation.

Automated summary

This study examined specific imitation deficits in patients with different forms of dementia and found that the patterns of deficits varied across different disease groups. The findings provide a new foundation for future research to investigate the underlying neurocognitive mechanisms responsible for specific imitation impairments.