Limb apraxia: cortical or subcortical.
Ideomotor apraxia is defined as a disturbance in timing, sequencing, and spatial organization of gestural movements. Left hemisphere motor dominance reflected by ideomotor apraxia mainly refers to spatially and temporally complex movements performed outside the natural context. While clinicoanatomical studies have failed to unveil a specific lesion correlating with apraxia, white matter damage-interrupting corticocortical and corticosubcortical connections-seems crucial for the deficit to be persistent and severe. Patients with basal ganglia lesions and disorders, such as Parkinson's disease and progressive supranuclear palsy, may exhibit ideomotor apraxia. The putative roles of the basal ganglia in object-oriented action, and therefore in praxis, would include among others (a) the selection of the kinematic parameters and the direction of arm movements, (b) working as an integral part of brain systems involved in timing and representation of action sequences, (c) encoding behavioral context, and (d) working as a subcortical component of the parietofrontal circuits devoted to sensorimotor transformation (e.g., reaching). Several studies suggest that basal ganglia pathology per se may not cause overt apraxia. However, when it is combined with dysfunction of the cortical components of the neural systems involved in sequencing, sensorimotor transformation, and response selection, different types of ideomotor praxis deficits would become clinically manifested.
Leiguarda
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Raúl Carrea Institute of Neurological Research, FLENI, Buenos Aires, Argentina. rleiguar@fleni.org.ar
D020240:Apraxia, Ideomotor / Q000175:diagnosis / Q000503:physiopathology*; D001479:Basal Ganglia / Q000503:physiopathology*; D001931:Brain Mapping; D002540:Cerebral Cortex / Q000503:physiopathology*; D004292:Dominance, Cerebral / Q000502:physiology; D006801:Humans; D009434:Neural Pathways / Q000503:physiopathology; D010300:Parkinson Disease / Q000175:diagnosis / Q000503:physiopathology; D011597:Psychomotor Performance / Q000502:physiology