Introduction

The term apraxia was introduced by Liepmann in 1908 (Liepmann, 1908) in order to describe an inability to properly execute a learned skilled movement which cannot be accounted for by weakness, incoordination or sensory deafferentation, or by language comprehension deficits or a global intellectual impairment. All patients described by Liepmann had suffered strokes in parietal or frontal regions. Although described in the early twentieth century, the clinical features of apraxia remain relatively unknown. Two old ideas contribute to underestimation of the critical role of apraxia after a stroke: the first is related to the concept that apraxia spontaneously and rapidly improves after a stroke, and the second is that, in view of the dissociation between automatic and voluntary motor skills, repercussion of apraxia in everyday life is mild.

Nevertheless, systematic studies of apraxia lead to different conclusions. For example, Basso et al. (1987) re-examined after several months 26 patients with focal left hemisphere vascular lesions who presented with ideomotor apraxia (IMA) in the acute period. They had to imitate 24 meaningful or meaningless movements with the hand ipsilateral to the lesion. The first examination was performed at between 15 and 30 days post-stroke, the second assessment at between 5 and 23 months. On the second examination the improvement was significant but half of the patients were still apraxic. Eleven of the 13 subjects were examined a third time. Five patients (1/4) presented with long-lasting apraxia (from 13.5 to 60 months after the stroke).