The basal ganglia and apraxia

Area of Science:

• Neuroscience
• Neurology
• Cognitive Science

Background:

• Apraxia is traditionally linked to cortical damage.
• Subcortical lesions, specifically in the basal ganglia and thalamus, have been suggested as potential causes of apraxia.
• Understanding the precise neuroanatomical correlates of apraxia is crucial for diagnosis and treatment.

Purpose of the Study:

• To investigate whether deep subcortical lesions in the basal ganglia or thalamus can cause apraxia.
• To analyze the characteristics of apraxias associated with deep brain lesions.
• To determine the specific roles of basal ganglia and thalamic nuclei in motor planning.

Main Methods:

• Meta-analysis of 82 reported cases of 'deep' apraxias.
• Classification of lesions based on size, location (basal ganglia, thalamus, white matter), and involvement of adjacent structures.
• Review of neuropathological studies and neuroimaging (CT/MRI) findings.

Main Results:

• Lesions confined solely to basal ganglia nuclei rarely cause apraxia; adjacent white matter involvement is often necessary.
• Lesions in the lenticular nucleus or putamen, with extension into periventricular or peristriatal white matter, frequently result in apraxia.
• Thalamic lesions can cause apraxia, even without apparent white matter involvement.
• Most cases occurred in the dominant (left) hemisphere, with ideomotor apraxia being the most common type.

Conclusions:

• Deep subcortical lesions, particularly those involving white matter tracts connected to the basal ganglia, are significant causes of apraxia.
• The thalamus plays a role in motor control and can induce apraxia when damaged.
• Further research is needed to fully elucidate the thalamus's role in apraxia and to define conditions like limb-kinetic apraxia.