What is the typical localisation of apraxia in the brain?

Localization of Apraxia in the Brain

Apraxia is predominantly localized to the left (dominant) hemisphere, with limb apraxia most commonly resulting from left-hemisphere stroke rather than right-hemisphere stroke. 1, 2, 3

Primary Anatomical Localization

Left Hemisphere Dominance

• Limb apraxia occurs more frequently after left hemispheric stroke than right hemispheric stroke, establishing clear left-hemisphere dominance for skilled motor planning and execution 1, 2, 3
• The left hemisphere's dominance applies to both meaningful and nonsense movements, indicating this lateralization is not dependent on the meaningfulness of the action 4
• This left-hemisphere specialization reflects control over movements performed to command and out of natural context, particularly those with increased spatial and temporal complexity 4

Specific Regional Involvement

Left Inferior Parietal Lobe:

• The left inferior parietal lobe plays a critical role in tool and body representation, action prediction, and action selection 5
• Parietal lesions produce characteristic patterns of apraxic deficits related to these specific functions 5

Distributed Network Architecture:

• Apraxia results from damage to various loci within a densely interconnected network spanning the left temporal, parietal, and frontal lobes 5
• The disorder reflects disruption of a complex distributed network involving dorsolateral prefrontal cortex, supplementary motor areas, anterior cingulate regions, and lateral premotor cortex 6

Subcortical Considerations

Basal Ganglia and White Matter

• Lesions confined purely to basal ganglia structures (putamen, caudate nucleus, globus pallidus) rarely, if ever, cause apraxia 6
• When apraxia appears with basal ganglia lesions, there is nearly always extension into adjacent lateral white matter, particularly involving the superior longitudinal fasciculus and frontostriatal connections 6
• Periventricular or peristriatal white matter involvement is the critical factor—white matter lesions alone can cause apraxia even when basal ganglia are spared 6
• Among 82 analyzed cases, only 8 showed apraxia with deep basal ganglia lesions apparently sparing white matter 6

Thalamic Involvement

• Thalamic lesions can sometimes cause apraxia (26 of 82 cases), even without apparent white matter involvement 6
• Small lesions confined to the thalamus occasionally produce apraxia (8 cases), though the thalamus's precise role in motor control and apraxia remains incompletely understood 6

Apraxia of Speech Localization

Apraxia of speech represents a motor planning or programming disorder affecting voluntary speech sound production, typically co-occurring with nonfluent aphasia 1, 2

• Nonfluent/agrammatic variant primary progressive aphasia (nfvPPA) is associated with frontotemporal lobar degeneration pathology, most commonly primary tauopathies such as progressive supranuclear palsy or corticobasal degeneration 1
• The existence of pure apraxia of speech without accompanying aphasia remains debatable, reflecting the overlapping neural substrates 1

Clinical-Anatomical Correlations

Corticobasal Syndrome

• Apraxia is a hallmark of corticobasal degeneration (CBD), characterized by various forms affecting limb function, particularly ideomotor and limb-kinetic apraxia 7
• The corticobasal syndrome involves both cerebral cortical sites and basal ganglia structures, though the diffuse involvement complicates precise localization 7

Posterior Cortical Involvement

• Progressive visuospatial dysfunction (posterior cortical atrophy syndrome) presents with limb apraxia alongside visual/spatial deficits, alexia, agraphia, and acalculia, usually due to Alzheimer's disease pathology affecting posterior cortical regions 1

Critical Caveats

No specific lesion locus within the left hemisphere consistently predicts the severity of ideomotor apraxia 4, reflecting the distributed nature of the motor planning network rather than a single critical site.

The term "apraxia" has been inconsistently applied to various motor disturbances (e.g., "gait apraxia," "apraxia of eyelid opening") that may be misnomers, demonstrating lack of coherent nomenclature in this field 7.