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Neurologists are familiar with the standard definition of apraxia: ‘an inability to perform a motor task that cannot be adequately explained by motor weakness, sensory loss or a lack of understanding’. Being a definition of exclusion, this has led to a bewildering number of motor disorders being described as forms of apraxia, despite many of these failing to capture the essence of what apraxia really is: a disorder of motor cognition. Apraxia reflects an impairment of the storage and transformation of motor representations in the brain, either through degradation of the semantic knowledge of gestures and tool use or through inability to translate the neural representations of higher level goals accurately into lower level patterns of muscle activation and inhibition.
Our current clinical approach to apraxia is similar to that proposed by Liepman in the early 20th century.1 He recognised that left hemispheric lesions tend to cause bilateral upper limb apraxia and suggested a model of motor control in which the left parietal lobe stores a ‘space–time form picture’ of a movement. For a movement to be executed, its picture must be retrieved and activated and then be associated via cortical projections with the relevant motor engrams in the prefrontal regions. From here the information passes to the primary motor cortex before being fed down the corticospinal tracts. For the right upper limb to move the information remains contained within the left hemisphere, but for the left upper limb to move the information from the left parietal lobe must first be sent to the right prefrontal and frontal regions through the corpus callosum.
Using this scheme, Liepman delineated three forms of apraxia. He described ideational apraxia as a disruption of the space–time picture, in which the idea of the movement itself is lost or degraded. In ideomotor apraxia, …
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