ABSTRACT
Limb apraxia is defined operationally as a disorder of learned skilled movement that cannot be explained by an elemental motor deficit such as weakness, akinesia, abnormalities of tone or posture, ataxia, movement disorders, or by intellectual deterioration, lack of understanding or uncooperativeness (Heilman & Rothi, 1993). The production and/or conceptual impairments observed in limb apraxia represent a disruption in the praxis system which normally is responsible for storing skilled motor information for future use. This complex system facilitates our interaction with the environment by providing a processing advantage for previously constructed programs rather than recreating the programs de novo each time they are required (Rothi, Ochipa, & Heilman, 1991). Localisation and information-processing models of apraxia suggest that the neural networks that mediate praxis are lateralised to the left hemisphere in most right-handers (Liepmann, 1977; Heilman, Rothi, & Valenstein, 1982). Impairment to the complex, multicomponant praxis system results in a variety of deficits, presumably dependent upon which components are compromised (Geschwind, 1965, 1975; Ochipa and Heilman, 1991, Roy & Square, 1985).
