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A view of apraxia
A previous exposition of apraxia in Practical Neurology1 offered an account of underlying impairment and accompanying clinical assessment based on a distinction between ideational, ideomotor and limb-kinetic apraxia. This conceptualisation stems from 19th-century models of higher cortical motor, language and visual function, revived by Geschwind2 3 in the 1960s. Liepmann in 19004 had posited a hierarchical model of action control over three discrete levels. At the top, movement formulae (‘visual engrams’ of the action) provided overall targets, which activate innervatory patterns to stimulate the appropriate muscles, coordinated contraction of muscles then led to execution of the action. (1) Ideational apraxia arose when movement formulae were either impaired or disconnected from the innervatory patterns. (2) Ideomotor apraxia resulted from disruption to innervatory patterns. (3) Limb-kinetic apraxia, assumed to be a disruption to the smooth neural transmission of the motor commands, was, even for Liepmann, not a full apraxia. It existed between apraxia and paresis only within a broader view of dysfunction.
Liepmann’s model proved valuable in studying apraxia. However, despite surviving in several neurology textbooks, the ideational–ideomotor dichotomy has now been replaced as a way of understanding and classifying apraxias,5–8 similar to the disbandment of Broca’s versus Wernicke’s aphasia, or the dichotomy of associative versus apperceptive agnosia9 (although these distinctions, too, still persist in some areas of clinical practice).
A radical rethink was needed, owing to issues with the underlying theoretical model of apraxia and difficulties in distinguishing between ideational and ideomotor clinically. Goldenberg7 made the plea to ‘relegate the dichotomy of ideational …
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