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Apraxia in deep cerebral lesions
Journal of Neurology, Neurosurgery, and Psychiatry
|September 1, 1983
Summary
Apraxia, a motor disorder, can result from subcortical brain lesions, not just cortical damage. This study found apraxia in patients with basal ganglia and thalamus lesions, challenging previous assumptions about its origin.
Area of Science:
- Neuroscience
- Neurology
- Clinical Neuropsychology
Background:
- Apraxia is traditionally considered a disorder of high cerebral (cortical) function.
- The precise neural substrates underlying different types of apraxia are still under investigation.
- Cerebrovascular lesions are a common cause of neurological deficits, including apraxia.
Purpose of the Study:
- To investigate the relationship between subcortical cerebrovascular lesions and the occurrence of apraxia.
- To determine if lesions in the basal ganglia and/or thalamus can cause apraxia.
- To challenge the exclusive cortical localization of apraxia.
Main Methods:
- Retrospective analysis of 50 patients with cerebrovascular lesions confirmed by CT scan.
- Identification of patients with lesions in the basal ganglia and/or thalamus.
- Clinical assessment of apraxia subtypes (ideomotor, constructional, bucco-facial, utilisation) in affected patients.
Main Results:
- Seven out of 50 patients had cerebrovascular lesions in the basal ganglia and/or thalamus.
- All seven patients with subcortical lesions presented with apraxia.
- Ideomotor apraxia was universal; constructional and bucco-facial apraxia were also observed, but not utilisation apraxia.
Conclusions:
- Apraxia can result from damage to subcortical structures, specifically the basal ganglia and thalamus.
- The integrity of subcortical circuits is crucial for motor planning and execution, challenging the purely cortical model of apraxia.
- These findings expand our understanding of the neural basis of apraxia and its potential localization within the brain.